Presentation on theme: "Syncope A Diagnostic and Treatment Strategy"— Presentation transcript:
1Syncope A Diagnostic and Treatment Strategy Developed by:David G. Benditt, M.D Richard Sutton, DScMedUniversity of Minnesota Medical Center Royal Brompton Hospital, London, UK
2Presentation Overview Prevalence & ImpactEtiologyDiagnosis & Evaluation OptionsSpecific ConditionsTreatment OptionsInsights into more efficient and effective diagnosis and treatment of patients with syncope
4The Significance of Syncope The only difference betweensyncope and sudden deathis that in one you wake up.11 Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89:
5The Significance of Syncope Syncope is a relatively common problem that affects over 1 million people in the U.S. each year. Syncope accounts for 1 to 6% of hospital admissions and 3% of emergency room visits each year.1,2The incidence of syncope is greater than 500,000 new patients per year.1.National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 1997.2. Blanc J-J, L’Her C, Touiza A, et al. Prospective Evaluation and Outcome of Patients Admitted for Syncope Over a 1-Year Period. Eur Heart J, 2002; 23:3.Day SC, et al. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med 1982;73:15-23.4.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:1 National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 19972 Blanc J-J, L’her C, Touiza A, et al. Eur Heart J, 2002; 23:3 Day SC, et al, AM J of Med 19824 Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:
6Syncope Reported Frequency Individuals <18 yrsMilitary Population yrsIndividuals yrs*Individuals >70 yrs*15%20-25%16-19%23%Multiple reports have examined the frequency with which syncope occurs in various populations. This slide provides an overview of such findings. In essence the frequency with which syncope is reported to have occurred in various study groups is approximately 20%. The basis for syncope would be expected to differ substantially among these groups. Younger patients will have a greater proportion of vasovagal syncope, whereas older individuals may reasonably be expected to have a higher likelihood of underlying structural heart disease, and hence a greater predilection to more worrisome etiologies.Brignole M, Alboni P, Benditt DG, et al. “Guidelines on Management (Diagnosis and Treatment) of Syncope. Eur Heart J 2001; 22:*during a 10-year periodBrignole M, Alboni P, Benditt DG, et al. Eur Heart J, 2001; 22:
7The Significance of Syncope explained: 53% to 62%infrequent, unexplained: 38% to 47% 1-4Studies have shown that the cause of syncope remains undiagnosed in as many as 47% of the patients who present with this symptom.There are approximately 170,000 recurrent syncope patients in the U.S. today, meaning that up to 70,000 patients with recurrent, infrequent syncope may be going undiagnosed and therefore, improperly treated.Of these patients, 20,000 may have undergone extensive testing with no diagnosis.1.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:2.Silverstein M, et al. Patients with syncope admitted to medical intensive care units. JAMA 1982;248:3.Martin G, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13:4.Kapoor W, et al. A prospective evaluation and follow-up of patients with syncope. N Eng J Med 1983;309:5.National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.6.Kapoor W, et al. Diagnostic and prognostic implications of recurrences in patients with syncope. Am J Med 1987;83:500,000 new syncope patients each year 5170,000 have recurrent syncope 670,000 have recurrent, infrequent, unexplained syncope 1-41 Kapoor W, Med. 1990;69:2 Silverstein M, et al. JAMA. 1982;248:3 Martin G, et al. Ann Emerg. Med. 1984;12:4 Kapoor W, et al. N Eng J Med. 1983;309:5 National Disease and Therapeutic Index, IMS America, Syncope and Collapse #780.2; Jan 1997-Dec 1997.6 Kapoor W, et al. Am J Med. 1987;83:
8The Significance of Syncope Some causes of syncope are potentially fatalCardiac causes of syncope have the highest mortality ratesCardiac causes include both arrhythmias and structural heart problems, both of which contribute to high mortality rates. One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders.Syncope is a serious clinical problem with a reported mortality and major morbidity rate of over 7%.1 Among patients with an underlying cardiac cause of syncope, the reported 1-year mortality rate ranges from 18 to 33%.1-4This means that within 5 years, most of the patients whose syncope has a cardiac cause will have died.1.Day SC, et al. Evaluation and outcome of emergency room patients with transient loss of consciousness. Am J Med. 1982;73:15-23.2.Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:3.Silverstein M, Singer D, Mulley A. Patients with syncope admitted to medical intensive care units. JAMA. 1982;248:4.Martin G, Adams S, Martin H. Prospective evaluation of syncope. Ann Emerg Med. 1984;13:1 Day SC, et al. Am J of Med 1982;73:15-23.2 Kapoor W. Medicine 1990;69:3 Silverstein M, Sager D, Mulley A. JAMA ;248:4 Martin G, Adams S, Martin H. Ann Emerg Med. 1984;13:
9Impact of Syncope 73% 1 71% 2 60% 2 Proportion of Patients 37% 2 Syncope result in substantial cost to patients and to society. For example, syncope patients live with lifestyle altering restrictions that affect daily activities, mobility, and employment. In addition, syncope and falling in the elderly commonly cause injury, institutionalization and premature death. Falls directly or indirectly cause 12% of deaths in geriatric population. (Baraff 1997).____________________Linzer M, Pontinen M, Gold DT, et al. Impairment of physical and psychological function in recurrent syncope. J Clin Epidemiol. 1991;44:Linzer M, Gold DT, Pontinen M, et al. Recurrent syncope as a chronic disease: Preliminary validation of a disease-specific measure of functional impairment. J Gen Int Med. 1994;9:Anxiety/ DepressionAlter Daily ActivitiesRestricted DrivingChange Employment1Linzer, J Clin Epidemiol, 1991.2Linzer, J Gen Int Med, 1994.
11Syncope: A Symptom…Not a Diagnosis Self-limited loss of consciousness and postural toneRelatively rapid onsetVariable warning symptomsSpontaneous complete recoverySyncope should be considered as a symptom not as a diagnosis. The basis of syncopal symptoms should be sought through careful evaluation. Only after a cause is established can an effective treatment regimen be developed.
12Causes of Syncope1 Cause Prevalence (Mean) % Prevalence (Range) % Reflex-mediated:Vasovagal188-37Situational51-8Carotid Sinus10-4Orthostatic hypotension84-10Medications31-7Psychiatric2Neurological103-32Organic Heart Disease4Cardiac Arrhythmias144-38Unknown3413-41These frequencies cited were based on the general experience reported in the literature at the time (circa 1998). Subsequently, diagnostic criteria and techniques have improved. Consequently, the numbers should be relied on only for “ballpark” estimates.1Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.
13Syncope: Etiology Neurally- Mediated Orthostatic Cardiac Arrhythmia StructuralCardio-PulmonaryNon-Cardio-vascular1VasovagalCarotid Sinus• SituationalCoughPost-micturition2DrugInduced• ANSFailurePrimarySecondary3BradySick sinusAV block• TachyVTSVTLong QT Syndrome*4Aortic StenosisHOCM• PulmonaryHypertension5Psychogenic• Metabolice.g. hyper-ventilationNeurologicalThis slide provides a simple classification of the principal causes of syncope. This scheme lists the causes of syncope from the most commonly observed (Left) to the least common (Right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients.Within the boxes,the most common causes of syncope are indicated for each of the major diagnostic groups. The numbers at the bottom of each column provide an approximate value for the average frequency (Kapoor 1998) with which that category appears in published reports summarizing diagnostic findings. It should be noted that orthostatic causes are not often referred to specialists and consequently tend to be under represented in the literature.24%11%14%4%12%Unknown Cause = 34%DG Benditt, UM Cardiac Arrhythmia Center
14Causes of Syncope-like States Migraine*Acute hypoxemia*Hyperventilation*Somatization disorder (psychogenic syncope)Acute Intoxication (e.g., alcohol)SeizuresHypoglycemiaSleep disorders* may cause ‘true’ syncope
16Syncope Diagnostic Objectives Distinguish ‘True’ Syncope from other ‘Loss of Consciousness’ spells:SeizuresPsychiatric disturbancesEstablish the cause of syncope with sufficient certainty to:Assess prognosis confidentlyInitiate effective preventive treatmentSyncope is often confused with other apparent loss of consciousness diagnoses. It is crucial to consider this distinction first, prior to embarking on a diagnostic evaluation.
17Initial Evaluation (Clinic/Emergency Dept.) Detailed historyPhysical examination12-lead ECGEchocardiogram (as available)The first steps in the evaluation of the patient with syncope can be carried out in the clinic (The Initial Evaluation). A detailed medical history (especially focusing on syncope events) and careful physical examination often provide important clues. A 12-lead ECG and if necessary an echocardiogram are reasonably included at this stage. A careful Initial Evaluation may often provide a satisfactory diagnosis. In other cases, this Evaluation will permit more development of a cost-effective diagnostic strategy.
18Syncope Basic Diagnostic Steps Detailed History & PhysicalDocument details of eventsAssess frequency, severityObtain careful family historyHeart disease present?Physical examECG: long QT, WPW, conduction system diseaseEcho: LV function, valve status, HOCMFollow a diagnostic plan...General rules for initiating the diagnostic evaluation of the syncope patient. The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.
19Conventional Diagnostic Methods/Yield Test/ProcedureYield(based on mean time to diagnosis of 5.1 months7History and Physical(including carotid sinus massage)49-85% 1, 2ECG2-11% 2Electrophysiology Study without SHD*11% 3Electrophysiology Study with SHD49% 3Tilt Table Test (without SHD)11-87% 4, 5Ambulatory ECG Monitors:Holter2% 7External Loop Recorder(2-3 weeks duration)20% 7Insertable Loop Recorder(up to 14 months duration)65-88% 6, 7Neurological †(Head CT Scan, Carotid Doppler)0-4% 4,5,8,9,10A yield is defined as information that will point to more finely focused tests, specialties, or treatments.Patient history and physical exam are the most productive diagnostic tools for recurrent syncope, accounting for 49-85% of all syncope diagnoses.1,2 An ECG, also considered a first-line test, is diagnostic in 2-11% of cases.2Beyond that, other tests have variable diagnostic yields. Holter monitors (worn for 1-3 days) capture ECGs during a syncopal episode in only 1% of patients, based on a mean time to recurrent event of 5.1 months.7The effectiveness of tilt table tests, a common tool used to identify vasovagal syncope, depends on several factors, including patient selection and use of provocative drugs. Depending on these factors, the rate of positive tests has been reported in the range of 11-87%.3,5 However, about 10% or more of the population (who do not experience syncope) will have positive tilt table tests.4,6External loop recorders (worn for 2-3 weeks) are most productive in motivated patients who experience relatively frequent syncope. They provide a diagnostic yield of 20%.7Electrophysiology (EP) studies are generally more productive in patients with structural heart disease (SHD) and therefore are generally a higher priority for patients in this group.1EP studies are used to diagnose syncope by inducing symptoms under controlled conditions, thereby attaining a “presumptive” diagnosis.1EP testing usually fails to identify intermittent bradycardia as a cause of syncope (6%) and may sometimes reveal unrelated rhythm disturbances that may be mistakenly identified as the cause of syncope.21. Kapoor W, et al. A prospective evaluation and follow-up of patients with syncope. N Engl J Med 1983;309:2. Kapoor W. Diagnostic evaluation of syncope. Amer J Med 1991;90:3. Linzer M, et al. Clinical guideline: Diagnosing syncope: Part 2: Unexplained syncope. Ann Intern Med 1997;127:76-86.4. Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:5. Kapoor W. Evaluation and management of the patient with syncope. JAMA 1992;268:6. Krahn A, et al. The etiology of syncope in patients with negative tilt table and electrophysiological testing. Circulation 1995;92:Krahn A, Klein G, Yee R: Recurrent syncope. Experience with an implantable loop recorder. Cardiology Clinics 1997; 15(2):8. Eagle K,, et al. The Yale J Biol and Medicine. 1983; 56: 1-8.9. Day S, et al. Am J Med. 1982; 73:10. Stetson P, et al. PACE. 1999; 22 (part II): 782.Please also see:Brignole M, Alboni P, Benditt DG, et al. “Guidelines on Management (Diagnosis and Treatment) of Syncope. Eur Heart Journal 2001; 22:1 Kapoor, et al N Eng J Med, 1983.2 Kapoor, Am J Med, 1991.3 Linzer, et al. Ann Int. Med, 1997.4 Kapoor, Medicine, 1990.5 Kapoor, JAMA, 19926 Krahn, Circulation, 19957 Krahn, Cardiology Clinics, 1997.8 Eagle K,, et al. The Yale J Biol and Medicine. 1983; 56: 1-8.9 Day S, et al. Am J Med. 1982; 73:10 Stetson P, et al. PACE. 1999; 22 (part II): 782.* Structural Heart Disease† MRI not studied
20Syncope Evaluation and Differential Diagnosis History – What to Look forComplete DescriptionFrom patient and observersType of OnsetDuration of AttacksPostureAssociated SymptomsSequelaeA comprehensive Medical History is key to the cost-effective diagnostic assessment of syncope patients. Critical historical features that need to be sought are listed here.
2112-Lead ECG Normal or Abnormal? Short sampling window (approx. 12 sec) Acute MISevere Sinus Bradycardia/pauseAV BlockTachyarrhythmia (SVT, VT)Preexcitation (WPW), Long QT, BrugadaShort sampling window (approx. 12 sec)The 12-lead ECG samples only a brief period of the cardiac rhythm (about 12 s). Consequently, absence of an abnormal rhythm is not a useful observation.The 12-lead ECG may, however, offer some useful clues for the syncope evaluation. If present, the findings noted on this slide may help lead to the choice of appropriate additional tests.
22Carotid Sinus Massage Site: Method: Carotid arterial pulse just below thyroid cartilageMethod:Right followed by left, pause betweenMassage, NOT occlusionDuration: 5-10 secPosture – supine & erectCarotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective.Note that an abnormal response to CSM (I.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
23Carotid Sinus Syndrome (CSS) Carotid Sinus MassageOutcome:3 sec asystole and/or 50 mmHg fall in systolic blood pressure with reproduction of symptoms =Carotid Sinus Syndrome (CSS)ContraindicationsCarotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 monthsRisks1 in 5000 massages complicated by TIACarotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here has proven both safe and effective.Note that an abnormal response to CSM (I.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
24Conventional AECG Low Yield, Poor Symptom / Arrhythmia Concordance* 8 studies, 2612 patients19% pts had symptoms with AECGOnly 4% had arrhythmia with symptoms79% pts were without symptoms14% had arrhythmia despite absence of symptomsAmbulatory ECG recordings offer longer periods of ECG recording than are obtained by the conventional 12-lead ECG. Thus, the chance of detecting a transient arrhythmia is improved. Nonetheless, multiple studies indicate that conventional AECGs are not as effective as was once hoped. Newer AECG techniques are in evolution (e.g., implantable loop recorders [ILRs]), and their effectiveness may be greater (see RAST study slides).This slide summarizes data presented in an ACC/AHA Task Force report on AECG.Reference:Crawford MH, Bernstein SJ, Deedwania PC, et al, ACC/AHA Guidelines for Ambulatory Electrocardiography. J Am Coll Cardiol 1999;34: (Executive summary and recommendations. Circulation 1999;100:* ACC/AHA Task Force, JACC 1999;
25Ambulatory ECG Method Comments Holter (24-48 hours) Useful for infrequent eventsEvent RecorderLimited value in sudden LOCLoop RecorderImplantable type more convenient (ILR)Wireless (internet) Event MonitoringIn developmentThe various forms of Ambulatory ECG recording techniques currently available are listed in this slide. ILRs are currently available. Internet monitoring is just being initiated, and although very promising, its utility is as yet uncertain.
26Head-up Tilt Test (HUT) Unmasks VVS susceptibilityReproduces symptomsPatient learns VVS warning symptomsPhysician is better able to give prognostic / treatment adviceThe rationale for undertaking head-up tilt (HUT) testing in patients suspected of having vasovagal syncope is summarized here. In essence, the test may not only provide useful diagnostic information, but it also provides an opportunity for patients to become more familiar with the condition and its possible warning signs. The latter may prove to be of considerable diagnostic utility in many individuals.
27Head-Up Tilt Test (HUT) ECG leads and intra-arterial pressure tracing illustrating the final moments of a head-up tilt test just prior to induced syncope. Note that blood pressure tended to fall in advance of the bradycardia component. Later, even though the patient is returned to supine posture,and the heart rate returns to normal, it may take some time for the arterial pressure to fully recover. The latter is due to persistent vasodilatation which may disappear slowly.DG Benditt, UM Cardiac Arrhythmia Center
28Electroencephalogram Not a first line of testingSyncope from SeizuresAbnormal in the interval between two attacks – EpilepsyNormal – SyncopeNeurologic studies (Head CT/MRI, EEG) are rarely useful in the diagnostic evaluation of the basis for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, absent apparent abnormal neurologic signs, such testing should be relegated to low priority.
29Value of Event Recorder in Syncope Example of a symptomatic wide-QRS tachycardia recorded during a near syncope in a patient undergoing AECG monitoring.*Asterisk denotes event markerLinzer M. Am J Cardiol. 1990;66:
30Reveal® Plus Insertable Loop Recorder The Reveal® Plus Insertable Loop Recorder system offers long-term, continuous, subcutaneous ECG monitoring and event-specific recording. This implantable device is designed to improve patient compliance with long-term AECG monitoring.The system includes an implanted loop recorder, a hand-held patient Activator, and a programmer with telemetry head that communicates noninvasively with the implanted device.When a patient experiences an episode, the device stores an ECG using the Activator or through the use of a auto-activating feature.The Reveal® Plus ILR can monitor continuously for up to 14 months. The probability of capturing an event is high—approximately 65-88%.1,2The ECG captured during the episode may “reveal” the ECG during the patient’s episode or may allow the clinician to rule in or rule out arrhythmic causes.The stored ECG data is retrieved, viewed, and printed or saved to a disk, using a Medtronic 9790 programmer with a 9766 A or AL programmer head.The Reveal ILR can then be re-started for continued monitoring.Krahn A, et al. Final results from a pilot study with an insertable loop recorder to determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol, 1998;82:2. Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51Patient ActivatorReveal® Plus ILR9790 Programmer
31ILR Recordings* 56 yo woman with syncope accompanied with seizures. Infra-Hisian AV Block: Dual chamber pacemakerExamples of ECG recordings obtained by the Reveal® ILR system in 2 symptomatic patients. See associated text for details.65 yo man with syncope accompanied with brief retrograde amnesia.VT and VF: ICD and meds*Medtronic data on file
32Randomized Assessment of Syncope Trial Usual care including:External loop recorderTilt test, EPS and othersUnexplained Syncopeafter history, physical exam, ECG, HolterLow Risk (EF > 35%)ILRDiagnosis+-Tilt test, EPS, othersThe Randomized Assessment of Syncope Trial (RAST) utilized the Reveal® ILR system to provide diagnostic information in syncope patients in whom the basis for symptoms remained unknown despite careful initial evaluation. Unexplained syncope patients were enrolled after meeting the inclusion/exclusion criteria, and were then randomized to ILR implantation or usual care (primary strategy)If a patient did not receive a diagnosis in the primary strategy arm, they were asked if they would accept crossover to the other study arm.ReferenceKrahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.
33RAST Methods Prospective randomized trial Inclusion: Exclusion: 60 patients with unexplained syncope referred for cardiac investigationInclusion:Recurrent unexplained syncopeReferred to the arrhythmia service for cardiac investigationNo clinical diagnosis after history, physical, ECG and at least 24 hours of cardiac monitoringExclusion:LVEF < 35%Unable to give informed consentMajor morbidity precluding one year of follow-upA brief summary of RAST methodology is provided here. Inclusion and Exclusion criteria are noted.ReferenceKrahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.
34RAST Results Unexplained Syncope n=60 ILR n=30 Conventional Results of the initial phase of RAST are summarized here. Among patients randomized to ILR, there appeared to be greater diagnostic yield than in patients randomized to the conventional diagnostic pathway.In Follow-upn=3Diagnosedn=14Undiagnosedn=13Diagnosedn=6Undiagnosedn=24Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.
35RAST Crossover Results Unexplained Syncopen=6013/30Undiagnosed after monitoring6 accepted crossover to conventional24/30Undiagnosed after conventional21 accepted crossover to ILRIn RAST, patients who remained undiagnosed after completion of the first arm of the study (see preceding slide) were offered crossover to the other diagnostic strategy arm. Once again, ILR proved superior to the conventional diagnostic strategyDiagnosedn=1Undiagnosedn=5Diagnosedn=8Undiagnosedn=5In follow-upn=8Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.
36RAST - Diagnoses number of patients Results show patients implanted with the ILR are more likely to receive a diagnosis in any category.The ILR was almost 5 times better at detecting bradycardia compared to conventional testing.ReferenceKrahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation 2001;104:46-51Krahn A, Klein GJ, Skanes Y. Circulation 2001; 104:46-51.
37Conventional EP Testing in Syncope Limited utility in syncope evaluationMost useful in patients with structural heart diseaseHeart disease…… %No Heart disease…18-50%Relatively ineffective for assessing bradyarrhythmiasConventional EP testing (I.e.,EPS, electrical stimulation without autonomic studies such as HUT) has not been highly effective in substantiating a basis for syncope. In this regard, EPS has been more effective in patients with structural cardiovascular disease than in those with normal cardiovascular status. Further, EPS has been more effective in patients with tachyarrhythmias than in those with bradyarrhythmias.The most important findings at EPS in regard to the evaluation of syncope patients are listed on the next slide.Brignole M, Alboni P, Benditt DG, et al. “Guidelines on Management (Diagnosis and Treatment) of Syncope. Eur Heart Journal 2001; 22:Brignole M, Alboni P, Benditt DG, et al. Eur Heart Journal 2001; 22:
38EP Testing in Syncope: Useful Diagnostic Observations Inducible monomorphic VTSNRT > 3000 ms or CSRT > 600 msInducible SVT with hypotensionHV interval ≥ 100 ms (especially in absence of inducible VT)Pacing induced infra-nodal blockAlthough EPS may not be as helpful as was once thought in terms of the diagnostic evaluation of syncope patients, the findings listed here are of particular value
39International Study of Syncope of Uncertain Etiology ISSUE StudyInternational Study of Syncope of Uncertain EtiologyObjectives:Understand the mechanism of syncope in tilt-positive and tilt-negative (isolated) patientsUse the ILR to assess the correlation of rhythms captured during tilt testing and spontaneous recurrent episodesInclusion Criteria:Patients with three or more syncopal episodes in the last 2 yearsGroups matched in age, sex, history of syncope, ECG, Echo abnormalities, SHD and arrhythmiasMoya A. Circulation. 2001; 104:
40ISSUE Study Design Multicenter, prospective 111 syncope patients 3 episodes in 2 years, first and last episode >6 months apartHistory, physical exam, ECG, CSM, echo,Holter (24 hr), other tests as appropriateTilt test followed by implant of RevealInsertable Loop RecorderFollow-up to recurrent spontaneous episodeMoya A. Circulation. 2001; 104:
41ISSUE Study Results Results Tilt-Negative Syncope (Isolated) n=82 Tilt-Positive Syncopen=29Recurrent Event Occurrence (#)34% (28)34% (10)Mean Time to Recurrent Event(range)105 days (47-226)59 (22-98)ILR ECG Documented (#)29% (24)28% (8)Tachyarrhythmia2% (2)Bradycardia16% (13)21% (6)Sinus Brady3% (1)Sinus Arrest12% (10)17% (5)AV Block1% (1)Total Arrhythmic18% (15)Normal Sinus Rhythm11% (9)7% (2)Moya A. Circulation. 2001; 104:
42ISSUE Study Conclusions: Homogeneous findings from tilt-negative and tilt-positive syncope patients were observed (clinical characteristics and outcomes). Most frequent finding was asystole secondary to progressive sinus bradycardia, suggesting a neuromediated originIn this study tilt-negative patients had as many arrhythmias (18%) as tilt-positive patients (21%)In tilt-positive patients the spontaneous episode ECG was more frequently asystolic than what was predicted by tilt testMoya A. Circulation. 2001; 104:
43ISSUE Study Implications HUT outcome was not predictive of vasodepressor vs. cardioinhibitory responseBradycardia is common in spontaneous VVS - independent of HUT outcomeBradycardia is more prevalent in spontaneous events vs. HUT induced VVSClinical Implication: Consider a strategy of postponing treatment until a spontaneous episode can be documentedThe ISSUE study used ILR to assess diagnosis in patients with suspected vasovagal syncope who had undergone head-up tilt-table (HUT) testing. Findings revealed a much higher frequency of bradycardia in conjunction with spontaneous syncope than would have been predicted based on HUT findings.Reference:Moya A, Brignole M, Menozzi C, Garcia-Civera R, Tognarini S, Mont L, Botto G, Giada F, Cornacchia D, and ISSUE Investigators. Mechanism of syncope in patients with isolated syncope and in patients with tilt-positive syncope. Circulation 2001;104:Moya A. Circulation. 2001; 104:
44Symptom-Rhythm Correlation Auto ActivationPointPatient ActivationPointThe gold standard for determining if a syncope episode is due to an arrhythmia is to record the rhythm during symptoms (symptom rhythm correlation). The ILR may help rule-in or rule-out arrhythmogenic causes.This slide depicts findings from an ILR interrogation as they appear on the programmer screen. In order to view stored event data, one taps the screen with the touch pen on the area of the summary graph that one wishes to view in more detail. This takes the viewer to the first zoom level of the event ECG waveform data and centers the area of the event you tapped.To view the event in greater detail, one taps the screen over the ECG of interest.On-screen calipers are available at every zoom level to measure cycle length. Intervals can be measured in milliseconds or beats per minute.Note: A - represents auto activated eventP - indicates time patient activated the event
45Diagnostic Limitations Difficult to correlate spontaneous events and laboratory findingsOften must settle for an attributable causeUnknowns remain 20-30% 1Determining a definitive basis for syncope can often be frustrating. Patience is a necessity. However, not infrequently one must settle for the most reasonable ‘attributable’ cause.1Kapoor W. In Grubb B, Olshansky B (eds) Syncope: Mechanisms and Management. Armonk NY; Futura Publishing Co, Inc: 1998; 1-13.
46Unexplained Syncope Diagnosis History and Physical ExamSurface ECGENT EvaluationEndocrine EvaluationCV Syncope WorkupHolterELR or ILRTilt TableEchoEPSNeurological TestingHead CT ScanCarotid DopplerMRISkull FilmsBrain ScanEEGOther CV TestingAngiogramExercise TestSAECGSearching for a Diagnosis:Patients can enter the diagnostic process at various points based on their presenting symptoms and/or syncope-related injuries. Also, the process of deriving a diagnosis for syncope can vary from institution to institution. As noted earlier, the diagnosis of syncope begins with a patient history and physical, and a surface electrocardiogram recording.If this initial evaluation suggests a cardiovascular cause such as myocardial infarction or structural heart disease, an echocardiogram and EP study may be performed. If no diagnosis is reached with these tests, the physician may move to any of the following tests, in any order: tilt table testing, Holter monitor, external loop recorder (ELR), or Reveal® Plus Insertable Loop Recorder(IRL). If none of those tests yield a diagnosis, some tests may be performed repeatedly and/or other specialists might be consulted for further testing including: endocrinology, neurology, psychiatry, ENT, etc.If no structural cardiovascular problems are suspected, the physician may choose diagnostic testing based on suspected vasovagal etiology and frequency and severity of symptoms.New diagnostic tools, such as ILRs, will cause significant discussions about when to use them, given their high diagnostic yields and high patient compliance.NOTES:ECG: ElectrocardiogramEEG: ElectroencephalogramMRI: Magnetic Resonance ImagingEcho: EchocardiogramEP Study: Electrophysiology StudyMI: Myocardial InfarctionSHD: Structural Heart DiseaseENT: ears-nose-throatPsychological EvaluationAdapted from: W.Kapoor.An overview of the evaluationand management of syncope. From Grubb B, Olshansky B (eds)Syncope: Mechanisms and Management.Armonk, NY: Futura Publishing Co., Inc.1998.
47Typical Cardiovascular Diagnostic Pathway SyncopeHistory and Physical, ECGKnown SHDNo SHD> 30 days; > 2 Events< 30 daysEchoThis flow chart shows a typical sequence of testing, patients may undergo in search of a diagnosis.SHD (Structural Heart Disease)EPSTilt Holter/ ELR ILRTilt ILR-+Tilt/ILRTreatAdapted from:Linzer M, et al. Annals of Int Med, :76-86.Syncope: Mechanisms and Management. Grubb B, Olshansky B (eds) Futura Publishing 1999Zimetbaum P, Josephson M. Annals of Int Med, :Krahn A et al. ACC Current Journal Review,1999. Jan/Feb:80-84.
48Section IV: Specific Conditions The next session of this set deals with some of the more important causes of syncope. Specific conditions are dealt with approximately in the order of the frequency with which they may be expected to occur in clinical practice.
49Neurally-Mediated Reflex Syncope (NMS) Vasovagal syncope (VVS)Carotid sinus syndrome (CSS)Situational syncopepost-micturitioncoughswallowdefecationblood drawingetc.The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation.Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur from time-to-time and are usually recognized only if a detailed medical history is obtained.
50NM Reflex Syncope: Pathophysiology Multiple triggersVariable contribution of vasodilatation and bradycardiaNeurally-mediated reflex syncope can be triggered by a wide variety of situations (thus the commonly used term ‘situational’ syncope). Extended periods of upright posture, and medical procedures, are among the more common situations associated with vasovagal faints.
51NMS – Basic Pathophysiology Cerebral CortexVascular BedBradycardia/ HypotensionBaro-receptorsHeartFeedback via Carotid Baroreceptors Other MechanoreceptorsParasympathetic (+)sympathetic (+)¯ Heart Rate ¯ AV Conduction_VasodilatationPhysiology of FaintingThe physiology of the common faint is depicted graphically in this slide (based on Figure 1 in Benditt 1996). The afferent trigger signals (e.g., pain, emotional upset, dehydration) are not depicted. The efferent loop of the neural reflex comprises:Parasympathetic signals from the cerebral cortex drive heart rate down and slow (or even block) AV conduction.Sympathetic signals increase dilation of the vascular bed.Bradycardia and/or hypotension result.Carotid baroreceptors and other mechanoreceptors sense effects driven by parasympathetic and sympathetic systems and provide paradoxical feedback to the central nervous system.The result may be a downward spiral in heart rate and blood pressure leading to syncope.__________________Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996.Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996
52Vasovagal Syncope (VVS): Clinical Pathophysiology Neurally Mediated Physiologic Reflex Mechanism with two Components:Cardioinhibitory ( HR )Vasodepressor ( BP )Both components are usually presentSyncope in vasovagal fainters, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow.Hypotension is the result of 2 pathophysiologic components:1. Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature)2. VasodilatationThe relative contribution of these 2 components varies among patients
53Prevalence of VVS Prevalence is poorly known In general: Various studies report 8% to 37% (mean 18%) of cases of syncope (Linzer 1997)In general:VVS patients younger than CSS patientsAges range from adolescence to elderly (median 43 years)Pallor, nausea, sweating, palpitations are commonAmnesia for warning symptoms in older patientsPrevalence of VVSThe prevalence of VVS is poorly known.The published data that exists mostly dates from before the advent of tilt table testing.Linzer (1997) surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope.Standards for diagnosis and reporting still are emerging.It is generally recognized thatVVS patients usually are younger than CSS patients (age range is from adolescent to elderly, median 43 years)VVS is more common in females.____________________Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Into Med. 1997;126(12):
54Spontaneous VVS 16.3 sec Continuous Tracing 1 sec Example of marked bradycardia recorder during a spontaneous vasovagal faint. The asystolic periods may be impressive in their duration, but do not in themselves constitute an indication for cardiac pacing.Continuous Tracing1 secDG Benditt, UM Cardiac Arrhythmia Center
55Management Strategies for VVS Optimal management strategies for VVS are a source of debatePatient education, reassurance, instructionFluids, salt, dietTilt TrainingSupport hoseDrug therapiesPacingClass II indication for VVS patients with positive HUT and cardioinhibitory or mixed reflexManagement Strategies for VVSOptimal management strategies for VVS are a source of debate.Patient education, reassurance, and instruction. When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope.Control of fluids, salt, and diet may help reduce incidence.Support hose may limit blood pooling in the legs and feet.Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date/Pacing may benefit some patientsPacing today is generally considered a last resort unless the patient experiences prolonged asystole during episodes.Diagnosis of VVS with positive head-up tilt test and a cardioinhibitory or mixed reflex is a Class II indication for pacing.2 large randomized controlled trials support the utility of pacing in very symptomatic VVS patients
56VVS: Tilt-Training Objectives Technique Enhance Orthostatic Tolerance Diminish Excessive Autonomic Reflex ActivityReduce Syncope Susceptibility / RecurrencesTechniquePrescribed Periods of Upright PostureProgressive Increased DurationHead-up tilt testing (HUT) has proved to be of considerable clinical value in establishing susceptibility to VVS in syncope patients. As with any test, the observations during HUT must be considered in the light of all clinical data in a given patient.
57Carotid Sinus Syndrome (CSS) Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope)CSS may be an important cause of unexplained syncope / falls in older individualsCarotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals.The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slidesREFERENCEBrignole M, Alboni P, Benditt DG, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart Journal 2001; 22:
58Etiology of CSSSensory nerve endings in the carotid sinus walls respond to deformation“Deafferentation” of neck muscles may contributeIncreased afferent signals to brain stemReflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilationEtiology of CSSThe etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles:Sensory nerve endings in the carotid sinus walls respond to deformation.An increase in afferent traffic results in cardioinhibition and vasodilatation.Differentiation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.____________________Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R (eds). Armonk, NY: Futura, 1996, ppKenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the older patient. Kenny RA (ed). London: Chapman & Hall Medical, 1996, ppCarotid Sinus
59Carotid Sinus Hypersensitivity(CSH) Abnormal response to CSMAbsence of symptoms attributable to CSSCSH reported frequent in ‘fallers’ (Kenny)CSH CSSUnderlying Cause: Carotid Sinus Hypersensitivity (CSH)The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM).CSH is considered present when a 5-second massage results in either more than 3 seconds of asystole or more than a 50 mm/Hg fall in systolic blood pressure.CSH is a necessary but not a sufficient condition for diagnosing CSS. The latter refers to symptoms such as bradycardia, dizziness, pre-syncope, syncope, and falling resulting from a hypersensitive carotid sinus reflex (Katritsis 1991).Many subjects who exhibit CSH are free of symptoms and require no treatment. In one study, 38% of patients being catheterized for angiography responded positively to CSM (Brown 1980)._________________Brown KA, Maloney JD, Smith HC, et al. Carotid sinus reflex in patients undergoing coronary angiography: Relationship of degree and location of coronary artery disease to response to carotid sinus massage. Circulation. 1980; 62:Katritsis D, Ward DE, Camm AJ. Can we treat carotid sinus syndrome? PACE. 1991;14(9):Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R (eds). Armonk, NY: Futura, 1996, p. 138.
60CSS and Falls in the Elderly 30% of people >65 yrs of age fall each year1Total is 9,000,000 people in USAApproximately 10% of falls in elderly persons are due to syncope250% of fallers have documented recurrence3Prevalence of CSS among frequent and unexplained fallers unknown but…CSH present in 23% of >50 yrs fallers presenting at ER 3CSS and Falls in the ElderlyFalls are the leading cause of injury among the elderly. According to “Falling in the Elderly” (1995):30% of the population older than 65 years of age falls each year.In the U.S., that amounts to about 9,000,000 people.50% of these fallers have documented recurrence.8% of the population greater than 70 years of age visit an ER for a fall.40% of these visits result in hospitalization.What is the contribution of cardioinhibitory CSS to these falls? This is an area of active research, but already-published results are suggestive: In one study, 279 fallers 50 years or older presenting to an emergency room with frequent or unexplained falls (at least 3 in previous 12 months) underwent carotid sinus massage, and 65 (23%) exhibited cardioinhibitory carotid sinus hypersensitivity (Richardson 1997).____________________Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, December, 1995.Richardson DA, Bexton RS, Shaw FE, Kenny RA. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE March 1997 (Part II):1Falling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society,2 Campbell et al: Age and Aging 1981;10:3Richardson DA, Bexton RS, et al. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE 1997
62VVS: Pharmacologic Rx Salt /Volume Beta-adrenergic blockers Salt tablets, ‘sport’ drinks, fludrocortisoneBeta-adrenergic blockers1 positive controlled trial (atenolol),1 on-going RCT (POST)DisopyramideSSRIs1 controlled trialVasoconstrictors (e.g., midodrine)1 negative controlled trial (etilephrine)This slide summarizes the key pharmacologic treatment options in VVS patients. Salt/volume education in conjunction with reassurance and/or tilt-training are the primary treatment avenues. Drug therapy should be reserved as a second-line option.
63Midodrine for Neurocardiogenic Syncope Monthsp < 0.001Symptom – Free Interval18016014012010080604020FluidMidodrineFindings from a recent clinical trial in which salt/volume therapy and midodrine treatment were compared in VVS patients. Midodrine proved to be more effective than volume alone in this selected patient population.Journal of Cardiovascular Electrophysiology Vol. 12, No. 8, Perez-Lugones, et al.
64Role of Pacing in Treating VVS Status of Pacing in VVSPerception of pacing for VVS changing:VVS with +HUT and cardioinhibitory response a Class IIb indication1Recent clinical studies demonstrated benefits of pacing in select VVS patients:VPS IVASISSYDITVPS II –Phase IROME VVS TrialRole of Pacing in Treating VVSThe perception of pacing as therapy for selected VVS patients has been changing with increased understanding of the syndrome, improved diagnostic techniques (especially tilt testing), and the development of improved therapies.VVS with a positive head-up tilt test and a predominately cardioinhibitory response may be considered a Class II indication for pacing.DDD/DDI with rate hysteresis sometimes has been successful, although it suffers from limitations:It uses a hysteresis rate as a trigger and a relatively high lower rate for intervention.“False positives” may result in prolonged high rate intervention.In recent years, new rate drop therapies specifically designed for treatment of neurocardiogenic syncope have been introduced.1Gregoratos G, et al. ACC/AHA Guidelines for Implantation of Cardiac Pacemakers and Antiarrhythmic Devices. Circulation ; 97:
65Role of Pacing in Treating VVS Status of Pacing in VVSBenefits of specific device features evolving:Some success with DDD/DDI hysteresis 1“False positives” may result in prolonged high rate interventionTied to lower rate interventionRate drop therapies designed for treating VVS syncope appear to be successful 2-4Role of Pacing in Treating VVSThe perception of pacing as therapy for selected VVS patients has been changing with increased understanding of the syndrome, improved diagnostic techniques (especially tilt testing), and the development of improved therapies.VVS with a positive head-up tilt test and a predominately cardioinhibitory response may be considered a Class II indication for pacing.DDD/DDI with rate hysteresis sometimes has been successful, although it suffers from limitations:It uses a hysteresis rate as a trigger and a relatively high lower rate for intervention.Limited in response to “False positives”In recent years, new rate drop therapies specifically designed for treatment of neurocardiogenic syncope have been introduced.1 Sutton R, et al. Circulation ; 102:2 Connolly S, et al. J Am Coll Cardiol 1999; 33:16-20.3 Ammirati F, et al. Circulation. 2002; 104:4 Ammirati F, et al. NASPE Abstract #307. PACE, Vol. 24, April 2002, Part II.
66VPS-I Vasovagal Pacemaker Study I Study Design:54 patients randomized, prospective, single center27 DDD pacemaker with rate drop response (RDR)27 no pacemakerPatient Inclusion Criteria:6 syncopal events ever+HUTRelative bradycardia**a trough heart rate <60/min if no isoproterenol used, <70/min if up to 2 mcg/min isoproterenol used, or <80/min if over 2 mcg/min isoproterenol usedConnolly S, et al. J Am Coll Cardiol 1999; 33:
67Endpoints: Outcome: VPS- I Time to first syncope RESULTS PACEMAKER CONTROL(n=27)Number of patients w/syncopal recurrence6 (22%)19 (70%)Mean time to first recurrence (days)11254Relative risk reduction of syncope*85.4%-*2p =Connolly S, et al. J Am Coll Cardiol 1999; 33:
68VPS- I 100 90 80 Control (No Pacemaker) 70 60 Cumulative Risk (%) 50 4030Pacemaker20103691215Time in MonthsNumber At RiskCPConnolly S, et al. J Am Coll Cardiol 1999; 33:
69VPS-I Conclusion: Dual-chamber pacing with rate drop response reduces the likelihood of syncope in patientswith recurrent VVS.Connolly S, et al. J Am Coll Cardiol 1999; 33:
70VASIS Vasovagal Syncope International Study Study Design:42 patients, randomized, prospective, multicenter19 DDI pacemaker (80 bpm) with rate hysteresis (45 bpm)23 no pacemakerPatient Inclusion Criteria:> 3 syncopal events in 2 years and last event occurring within 6 months of enrollment and,Positive VASIS type 2A or 2B cardioinhibitory response to HUT and,Age > 40 years or drug refractory if < 40 yearsType 2A response is defined as the heart rate rising initially then falling to a ventricular rate <40 bpm for >10 sec or asystole occurring for >3 sec, with blood pressure rising initially then falling before the heart rate falls.Type 2B response is defined as the heart rate rising initially then falling to a ventricular rate <40 bpm for >10 sec or asystole occurring for >3 sec, with blood pressure rising initially and only falling to hypotensive levels <80 mmHg systolic at or after the onset of rapid and severe heart rate fall.Sutton, R, et al. Circulation ; 102:
71Endpoints: Outcome: VASIS Time to first syncope RESULTS Pacemaker No Pacemaker(n=23)Number of patients w/syncopal recurrence1 (5%)14 (61%)Median time to first recurrence (months)*155*P=Sutton, R, et al. Circulation ; 102:
72VASIS 100 Pacemaker 80 p=0.0004 % syncope-free 60 40 No-Pacemaker 20 2 The VASIS trial examined the effectiveness of cardiac pacing in patients with recurrent VVS symptoms and evidence of a bradycardiac component during evaluation.As was the case in the North American VPS1 study, pacing was more effective than conventional therapy in terms of preventing syncope recurrences.The VASIS intention-to-treat data are presented in Kaplan-Meier format.References:VASIS:Sutton R, Brignole M, Menozzi C, et al. Dual-chamber pacing is efficacious in treatment of neurally-mediated tilt-positive cardioinhibitory syncope. Pacemaker versus no therapy: a multicenter randomized study. Circulation 2000; 102:VPS1:Connolly SJ, Sheldon R, Roberts RS, Gent M, Vasovagal pacemaker study investigators. The North American vasovagal pacemaker study (VPS): A randomized trial of permanent cardiac pacing for the prevention of vasovagal syncope. J Am Coll Cardiol 1999; 33: 16-2023456Years7121415233140# of ptsSutton, R, et al. Circulation ; 102:
73VASISConclusion:Dual-chamber pacing (at a rate of 80 bpm ) with rate hysteresis reduces the likelihood of syncope in patients with tilt-positive, cardioinhibitory syncope.Sutton, R, et al. Circulation ; 102:
74SYDIT Syncope Diagnosis and Treatment Study Study Design:93 patients randomized, prospective, multicenter46 DDD pacemaker with rate drop response (RDR)47 Atenolol 100 MG/DPatient Inclusion Criteria:> 55 yrs> 3 syncopal episodes in 2 years+ HUT with relative bradycardia (trough HR <60 bpm)A recent study compared cardiac pacing (DDD mode with rate-drop response algorithm [RDR]) to beta-adrenergic blockade (atenolol 100 mgm daily) in older (>55 years) patients with VVS and evidence of bradycardia.The primary endpoint was time to first syncope recurrence.Ammirati F, et al. Circulation. 2001; 104:52-57.
75SYDIT Endpoints: Outcome: Time to first syncope RESULTS PACED (n= 46) DRUG(n= 47)Number of patients w/syncopal recurrence*2 (4%)12 (25%)Median time to first recurrence (days)390135Pacing proved to be more effective (see slide for data).REFERENCEAmmirati F, Colivicchi F, Santini M, et al. Permanent cardiac pacing versus medical treatment for the prevention of recurrent vasovagal syncope. A multicenter, randomized, controlled trial. Circulation 2001; 104: 52-56*P=0.004Ammirati, et al. Circulation. 2001; 104:52-57.
76Syncope-free Survival: Intention-to-Treat (n=46/paced, 47/drug). SYDITSyncope-free Survival: Intention-to-Treat (n=46/paced, 47/drug).1.00.9drugpacemaker0.8P =% of syncope free ptsData from the pacing vs. atenolol study discussed on the previous slide. Findings are depicted in terms of % patients remaining syncope-free vs. time (days). In general, pacemaker treated patients (pmk) had a longer symptom free interval than did drug treated patients.0.70.61002003004005006007008009001000Time (days)Ammirati F, et al. Circulation. 2001; 104:52-57.
77SYDITConclusion:Dual-chamber pacing + RDR is superior to Atenolol in prevention of recurrent syncope in highly symptomatic patients with relative bradycardia during tilt-induced syncope.Ammirati F, et al. Circulation. 2001; 104:52-57.
78VPS-II: Phase I Vasovagal Pacemaker Study-II Study Design:100 patients, randomized, prospective, multicenter50 DDD pacemaker with rate drop response (RDR)50 ODO pacemaker (inactive mode)Patient Inclusion Criteria:> 6 syncope events ever or > 3 syncope events in 2 years or > 1 syncope event in 6 months and,Positive HUT with syncope or presyncope and a heart rate blood pressure product <9000Presented at the 23rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11,
79VPS-II: Phase I Endpoints: Outcome: Time to first syncope RESULTS DDD Pacemaker(n= 50)ODO PacemakerNumber of patients w/syncopal recurrence16 (32%)22 (44%)Relative Risk Reduction*28.7%-*P=0.153Presented at the 23rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11,
80Cumulative Risk of Syncope VPS-II: Phase I0.40.3ODODDDCumulative Risk of Syncope0.2P = (one-sided)0.10.0123456ODODDDNumber at RiskPresented at the 23rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11,
81Conclusions: VPS-II: Phase I Lower than anticipated syncope event rate in the control arm.Higher than anticipated event rate in the treatment group.Consequence: treatment effect was less than VPS-I.Results favored pacing but the treatment effect was not statistically significant.Presented at the 23rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11,
82VVS Pacing Trials Conclusions DDD pacing reduces the risk of syncopein patients with recurrent, refractory,highly-symptomatic, cardioinhibitoryvasovagal syncope.
83SAFE PACE Study Design Randomized controlled trial (N=175): Pacing (87) vs. No Pacing (88)Single center: Royal Victoria Infirmary, Newcastle, UKRecruitment began: April 199812 month follow-up per patientStudy concluded: May 2000The study was a randomised controlled trial, pacing versus no pacing, performed at the Royal Victoria Infirmary in Newcastle, between April 1998 and May Patients were followed for 12 months after randomisation.Kenny RA, J Am Coll Cardiol 2001; 38:
84SAFE PACE Inclusion Criteria Consecutive adults attending accident and emergency department> 50 Years- Experienced non-accidental fallPositive response to CSMThe inclusion criteria were consecutive adults, over the age of 50 years, presenting with a non-accidental fall, and who exhibited a positive response to CSM and who had no evidence of cognitive impairment or dementia.Kenny RA, J Am Coll Cardiol 2001; 38:
85SAFE PACE Screening Process Accident and Emergency Attendees > 50 YrsFalls or SyncopeNon-accidental FallCSM PerformedThe study design is shown in the next slide. Patients presenting the A & E Department (or ER) were screened for falls or syncope, and non-accidental fallers identified. Carotid sinus massage was performed, and those patients who exhibited a cardioinhibitory or mixed (i.e. both vasodepressor and cardioinhibitory) response were randomised to either pacing or no specific intervention.Cardioinhibitory or Mixed CSHRCTControlPacemakerKenny RA, J Am Coll Cardiol 2001; 38:25
86SAFE PACE Screening Results RCT (n=175)Control (n=88)Pacemaker (n=87)Patients in the pacing arm of the study received a Medtronic DR pacemaker, containing the rate-drop response algorithm for syncope patients.No pacing interventionMedtronic Thera DR (Rate Drop Response Algorithm)Kenny RA, J Am Coll Cardiol 2001; 38:25
87SAFE PACE Results Number of Falls Controln=87Pacemakern=84% Participants w/Falls60%58%Total Number of Falls*699216Mean Number of Falls**9.34.170% Reduction [OR 0.42; 95% CI: 0.23, 0.75]However, there was a statistically significant reduction in the total number of falls among the pacemaker patient group, with a 70% reduction in total falls compared with the control group.* Falls during 12 months post randomization** Crude adjustment calculationKenny RA, J Am Coll Cardiol 2001; 38:
88SAFE PACE Results Number of Syncopal Episodes ControlN=87PacemakerN=84% Participants w/Syncopal Events22%11%Total Number of Syncopal Events4722Mean Number Syncopal Events1.140.2050% Reduction [OR 0.53; 95%CI 0.23; 1.20 ns]Only 28 patients reported syncope; 22 syncopal events were reported by paced patients and 47 by controls. Although there was a 50% reduction in the overall number of syncopal episodes, this did not reach statistical significance.* Syncopal events 12 months past randomization** Crude adjustment calculationKenny RA, J Am Coll Cardiol 2001; 38:
89SAFE PACE Results Number of Injury Events Controln= 87Pacemakern= 84% Participants w/Injurious Events41%35%Total Number Injury Events20261-Fractures-Soft Tissue Injury419835870% ReductionThere was also a reduction in the total number of injury events of 70%, from 202 in the control group to 61 in paced patients.* Injurious events 12 months post randomizationKenny RA, J Am Coll Cardiol 2001; 38:
90SAFE PACE Conclusions Falls by 70% Syncopal events by 53% In patients with unexplained falls and adiagnosis of Cardioinhibitory CSH, cardiacpacing reduced the total number of:Falls by 70%Syncopal events by 53%Injurious events by 70%In patients with unexplained falls and a diagnosis of cardioinhibitory carotid sinus hypersensitivity, cardiac pacing reduced the total number of falls by 70%, total syncopal events by 53% and total injurious events by 70%.Kenny RA, J Am Coll Cardiol 2001; 38:
91Role of Pacing in CSS -- Syncope Recurrence Rate Class I indication for pacing (AHA and BPEG)Limit pacing to CSS that is:CardioinhibitoryMixedDDD/DDI superior to VVI57%% RecurrenceRole of Pacing in Treatment of CSSCSS is a Class I indication for pacing (AHA and BPEG).Pacing therapy may be effective for CSS that is eitherCardioinhibitoryorMixed cardioinhibitory/vasodepressorAV sequential pacing (DDD/DDI) is clearly preferable to ventricular demand (VVI) pacing.____________________Wagshal AB, Wang SKS. Carotid sinus hypersensitivity. In: Syncope: Mechanisms and management. Grubb BP, Olshansky B (eds). Armonk, NY: Futura, 1998.Brignole M, Menozzi C. Carotid sinus syndrome: Diagnosis, natural history and treatment. Eur J C P E. 1992;4:%6(Mean follow-up = 6 months)Brignole et. Al. Diagnosis, natural history and treatment. Eur JCPE. 1992; 4:
92Section VI: Insights into More Efficient and Effective Diagnosis and Treatment
93Principal Causes of Orthostatic Syncope Drug-induced (very common)diureticsvasodilatorsPrimary autonomic failuremultiple system atrophyParkinsonismSecondary autonomic failurediabetesalcoholamyloidAlcoholorthostatic intolerance apart from neuropathyOrthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions.The most important conditions predisposing to orthostatic syncope are listed here.
94Syncope Due to Arrhythmia or Structural CV Disease: General Rules Often life-threatening and/or exposes patient to high risk of injuryMay be warning of critical CV diseaseAortic stenosis, Myocardial ischemia, Pulmonary hypertensionAssess culprit arrhythmia / structural abnormality aggressivelyInitiate treatment promptlySyncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem.
95Principal Causes of Syncope due to Structural Cardiovascular Disease Acute MI / IschemiaAcquired coronary artery diseaseCongenital coronary artery anomaliesHOCMAcute aortic dissectionPericardial disease / tamponadePulmonary embolus / pulmonary hypertensionValvular abnormalitiesAortic stenosis, Atrial myxomaA list of important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope is provided. The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
96Syncope Due to Cardiac Arrhythmias BradyarrhythmiasSinus arrest, exit blockHigh grade or acute complete AV blockTachyarrhythmiasAtrial fibrillation / flutter with rapid ventricular rate (e.g. WPW syndrome)Paroxysmal SVT or VTTorsades de pointesBoth excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm.
97Rhythms During Recurrent Syncope Bradycardia36%Normal Sinus Rhythm58%Normal Sinus Rhythm58%Tachyarrhythmia6%Krahn A, et al. Circulation. 1999; 99:
98AECG: 74 yr Male, SyncopeThis ambulatory ECG (AECG) recording was obtained in a patient being evaluated for recurrent syncope. The finding of an abnormal sinus pause provides presumptive evidence suggesting a basis for the symptoms. However, this is not definitive evidence unless the patient has reproduction of his usual symptoms at the time. Further, the pathophysiologic basis for the pause (i.e., intrinsic disease vs. neurally-mediated origin (e.g., carotid sinus syndrome) cannot be determined definitively from this recording alone.From the files of DG Benditt, UM Cardiac Arrhythmia Center
99Syncope: TorsadesTorsades de pointes ventricular tachycardia often presents as syncope, although life-threatening sustained tachyarrhythmias may also occur. The underlying factors are most often either acquired or congenital long QT syndrome.In this case, the patient had been treated with quinidine for several weeks in an attempt to suppress episodes of atrial fibrillation.From the files of DG Benditt, UM Cardiac Arrhythmia Center
10028 yo man in the ER multiple times after falls resulting in trauma VT: ablated and medicated83 yo womanBradycardia: Pacemaker implantedReveal® ILR recordings from patients with syncopal symptoms. The upper left recording was obtained in an 83 year old woman and suggests bradycardic episodes as a cause of syncope. The lower right recording was obtained in a younger patient with idiopathic ventricular tachycardiaReveal ® ILR recordings; Medtronic data on file.
101Infra-His BlockSyncope in this patient was due to intermittent AV block. This recording, obtained during EPS, reveals infra-His block. A pacemaker was implanted.From the files of DG Benditt, UM Cardiac Arrhythmia Center
102Drug-Induced QT Prolongation AntiarrhythmicsClass IA ...Quinidine, Procainamide, DisopyramideClass III…Sotalol, Ibutilide, Dofetilide, Amiodarone, (NAPA)Antianginal Agents(Bepridil)Psychoactive AgentsPhenothiazines, Amitriptyline, Imipramine, ZiprasidoneAntibioticsErythromycin, Pentamidine, FluconazoleNonsedating antihistamines(Terfenadine), AstemizoleOthers(Cisapride), DroperidolNumerous drugs have been associated with QT interval prolongation leading to susceptibility to torsade de pointes ventricular tachycardia. Certain of these agents have been removed from the market in the USA. These have been noted in parentheses.
103Treatment of Syncope Due to Bradyarrhythmia Class I indication for pacing using dual- chamber system wherever adequate atrial rhythm is availableVentricular pacing in atrial fibrillation with slow ventricular responseThe treatment of bradyarrhythmias associated with intrinsic conduction system disease resulting in syncope is usually cardiac pacing. On occasion, removal of an offending drug may be sufficient. The problem of neurally-mediated reflex bradyarrhythmias are dealt with separately.
104Treatment of Syncope Due to Tachyarrhythmia Atrial Tachyarrhythmias;AVRT due to accessory pathway – ablate pathwayAVNRT – ablate AV nodal slow pathwayAtrial fib– Pacing, linear / focal ablation, ICD selected ptsAtrial flutter – Ablation of reentrant circuitVentricular Tachyarrhythmias;Ventricular tachycardia – ICD or ablation where appropriateTorsades de Pointes – withdraw offending Rx or ICD (long-QT/Brugada)Drug therapy may be an alternative in many casesThis slide provides an overview of the multiple tachyarrhythmias that may cause syncope. EPS has proven more valuable in assessing tachyarrhythmia causes of syncope than those due to bradycardia.
105Conclusion Syncope is a common symptom, often with dramatic consequences,which deserves thorough investigationand appropriate treatment of its cause.
106Disclaimer INDICATIONS 9526 Reveal® Plus Insertable Loop Recorder The Reveal Plus Insertable Loop Recorder (ILR) is an implantable patient activated monitoring system that records subcutaneous ECG and is indicated for patients who experience transient symptoms that may suggest a cardiac arrhythmia.9790 ProgrammerThe Medtronic 9790 Programmers are portable, microprocessor based instruments used to program Medtronic implantable devices.6191 ActivatorThe Model 6191 Activator is intended for use in combination with a Medtronic Model 9525 Reveal® and the Model 9526 Reveal Plus Insertable Loop Recorders.CONTRAINDICATIONSThere are no known contraindications for the implantation of the Reveal Plus ILR. However, the patient’s particular medical condition may dictate whether or not a subcutaneous, chronically implanted device can be tolerated.WARNINGS/PRECAUTIONS9526 Reveal Plus Insertable Loop RecorderPatients with the Reveal Plus ILR should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation, electrosurgical cautery, external defibrillation, lithotripsy, and radiofrequency ablation to avoid electrical reset of the device, and/or inappropriate sensing.Operation of the Model 6191 Activator near sources of electromagnetic interference, such as cellular phones, computer monitors, etc., may adversely affect the performance of this device.See the appropriate technical manual for detailed information regarding indications, contraindications, warnings, and precautions.Caution: Federal law (U.S.A.) restricts this device to sale by or on the order of a physician.
107Disclaimer INDICATIONS Medtronic.Kappa 700 Series Pacemakers The Medtronic.Kappa 700 Series pacemakers are indicated for rate adaptive pacing in patients who may benefit from increased pacing rates concurrent with increases in activity and are also indicated for dual chamber and atrial tracking modes in patients who may benefit from maintenance of AV synchrony. Dual chamber modes are specifically indicated for treatment of conduction disorders that require restoration of both rate and AV synchrony, which include various degrees of AV block to maintain the atrial contribution to cardiac output and VVI intolerance (e.g., pacemaker syndrome) in the presence of persistent sinus rhythm.9790 ProgrammerThe Medtronic 9790 Programmers are portable, microprocessor based instruments used to program Medtronic implantable devices.9462The Model 9462 Remote Assistant is intended for use in combination with a Medtronic implantable pacemaker with Remote Assistant diagnostic capabilities.CONTRAINDICATIONSThe Medtronic.Kappa 700 Series pacemakers are contraindicated for the following applications:· Dual chamber atrial pacing in patients with chronic refractory atrial tachyarrhythmias.· Asynchronous pacing in the presence (or likelihood) of competitive paced and intrinsic rhythms.· Unipolar pacing for patients with an implanted cardioverter-defibrillator (ICD) because it may cause unwanted delivery or inhibition of ICD therapy.WARNINGS/PRECAUTIONSMedtronic.Kappa 700 Series patients should avoid sources of magnetic resonance imaging, diathermy, high sources of radiation, electrosurgical cautery, external defibrillation, lithotripsy, and radiofrequency ablation to avoid electrical reset of the device, inappropriate sensing and/or therapy.See the appropriate technical manual for detailed information regarding indications, contraindications, warnings, and precautions.Caution: Federal law (U.S.A.) restricts this device to sale by or on the order of a physician.
109Falls -- Incidence, Recurrence, CHS* 50% 130% 1Percent of People23% 2CSS and Falls in the ElderlyFalls are the leading cause of injury among the elderly. According to “Falling in the Elderly” (1995):30% of the population older than 65 years of age falls each year.In the U.S., that amounts to about 9,000,000 people.50% of these fallers have documented recurrence.8% of the population greater than 70 years of age visit an ER for a fall.40% of these visits result in hospitalization.Carotid sinus hypersensitivity and CSS increasingly are being recognized as attributable causes for unexplained falls and syncope in elderly patients. What is the contribution of CSS to these falls? This is an area of active research, but already-published results are suggestive: In one study, 279 fallers 50 years or older presenting to an emergency room with frequent or unexplained falls (at least 3 in previous 12 months) underwent carotid sinus massage, and 65 (23%) exhibited cardioinhibitory carotid sinus hypersensitivity (Richardson 1997).____________________Falling in the elderly: U.S. prevalence data. J Am Geriatr Soc, December, 1995.Richardson DA, Bexton RS, Shaw FE, et al. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the accident and emergency department with “unexplained” or “recurrent” falls. PACE. 1997;(Pt II):Incidence > 65 yrs. oldRecurrenceCSH* present in fallers > 50 yrs. presenting at ER1 Falling in the Elderly, 1995.2 Richardson, PACE, 1997.* Carotid Sinus Hypersensitivity
111Pacing in VVSTwo randomized, controlled trials suggest benefit in selected patients with multiple (>5 lifetime) syncope recurrences and one or more of:prominent cardioinhibitory featuresasystolic pause >10 secondssustained HR<40/minuteThe role of cardiac pacing in the treatment of VVS patients remains in evolution. However, to date 2 randomized controlled trials (RCTs) suggest that very symptomatic VVS patients may benefit from pacing. A third study (VPS2) has concluded, but the results are not yet made public
112VVS Recurrences35% of patients report syncope recurrence during follow-up ≤3 yearsPositive HUT with >6 lifetime syncope episodes: recurrence risk >50% over 2 yearsRecent studies suggest that VVS tends to recur in a substantial percentage of patients. Individuals who have historically experienced multiple syncopes over a long period of time are the ones at greatest risk of future recurrences.REFERENCE:Sheldon et al. Circulation 1996; 93:Savage et al. STROKE 1985; 16:Sheldon et al. Circulation 1996; 93:Savage et al. STROKE 1985; 16:
113SAFE PACE 2: Syncope and Falls in the Elderly 30% of individuals >65 yrs fall each year5% of falls result in fractures1% of falls result in hip fracturesSAFEPACE Pilot Study18% prevalence of CSH in unexplained ‘fallers’31% in ‘fallers’ >80 yrsRecent findings from the SAFEPACE study suggest that Falls are an important source of morbidity in older patients. Further, it appears that many ‘fallers’ may have clinical findings suggestive of Carotid Sinus Syndrome. If these findings are corroborated, cardiac pacing may prove to be important for preventing syncope and falls in the elderly.REFERENCEFalling in the Elderly: U.S. Prevalence Data. Journal of the American Geriatric Society, December, 1995.Richardson DA, Bexton RS, Shaw FE, Kenny RA. Prevalence of cardioinhibitory carotid sinus hypersensitivity in patients 50 years or over presenting to the Accident and Emergency Department with “unexplained” or “recurrent” falls. PACE March 1997 (Part II):820-23Kenny RA, J Am Coll Cardiol 2001; 38:
114Rate Drop Response Overview Detection OptionsDropDetectBothLow RateDetectRate Drop Detection in Medtronic Kappa® Series PacemakersRate Drop Response therapy has evolved as clinical experience has been gained. In the Medtronic Kappa Generation pacing system three detection options are available:Drop Detect. The Drop Detect algorithm detects a relative heart rate drop of a pre-determined size.Low Rate Detect. The Low Rate Detect algorithm works like rate hysteresis but with more flexibility, intervening after the heart rate falls to a user-defined lower rate for a programmed number of beats.Both. With this option, either criterion will trigger intervention. The Low Rate Detection algorithm provides back-up detection.When a Rate Drop Detection therapy is programmed, an automatic diagnostic records summary data. A clinician selectable diagnostic also is available to record beat-to-beat data for one episode.Detects relative heart rate drops of a pre-determined sizeDetection occurs when either Drop Detection or Low Rate Detection criteria are metDetects heart rate that falls to a user-defined lower rateRate Drop Detection in Medtronic Kappa® Series Pacemakers
115Drop Detection with Intervention Drop Detection Method: Drop Size 25, Drop Rate 70110100Peak Rate=90 bpm9080Drop Size=25 bpmVentricular RateRate Drop Detection in Medtronic Kappa® Series PacemakersDrop Detection allows the user to specify a relative drop in ventricular rate. Drop detection will only occur when two conditions are met:Drop Size: This is the size of the relative heart rate drop. Advance knowledge of the precise range of rates which will occur during a drop is not required to optimize the algorithm. To detect, the total ventricular rate drop must be greater than or equal to the user defined drop size. The “top” of the drop size is determined by the peak rate (defined on next slide)Drop Rate: Heart rate must be at or below this programmable rate for two consecutive beats for detection to occur.Fulfillment of these two criteria can occur in either order.In this slide, the heart rate has met the Drop Size and Drop Rate criteria and intervention has occurred.Note that in Medtronic Kappa®, 2 consecutive beats less than or equal to the Drop Size and Drop Rate triggers therapy. Two simplify programming, the number of “Confirmation Beats” is fixed at two based on prior physician experience.70Drop Rate602 consecutive beats<Drop50Size and Drop Rate40Rate Drop Detection in Medtronic Kappa® Series Pacemakers
116Drop Detect Peak Rate Drop Detection Method: Drop Size 25 120Peak Rate=90 bpm11010090Ventricular Rate80Drop Size=25bpm70Rate Drop Detection in Medtronic Kappa® Series PacemakersDetermination of Peak RateIn the Drop Detection detection algorithm, peak rate is determined as follows:The upper bound of the drop size is defined dynamically by the peak rate, which is the slower of two consecutive fastest beats during the detection window. This design avoids basing the peak rate on a PVC or a fast ventricular response to a PAC.The diagram shows an example. Following detection, intervention therapy is applied at a programmed rate for a programmed period of time.605040Rate Drop Detection in Medtronic Kappa® Series Pacemakers
117Low Rate DetectLow Rate Detection Method: Lower Rate 40, Detection beats 21101009080Ventricular Rate70Rate Drop Detection in Medtronic Kappa® Series PacemakersThe Low Rate Detection algorithm detects when the heart rate falls to a user-defined lower rate. It is important to note that the lower rate in the RDR Low Rate Detection method is the same as the pacemaker programmed lower rate. Low Rate Detection works as follows:The pacemaker intervenes when lower rate pacing occurs for a programmable number (1 to 3) of beats, as defined by the Detection Beats parameter. When Detection Beats = 2 or 3, intervention cannot be triggered by a single slow beat, such as a compensatory pause following a PVC.Intervention Rate and Duration are programmable, as with Drop Detection.This slide provides an example of Low Rate Detection and subsequent intervention.A cautionary note with the Low Rate Detection option:This method is contraindicated in patients who require low rate pacing support due to bradyarrhythmias.If patients do not require low rate pacing support, Low Rate Detection should be set below the lowest daily heart rate (<50ppm) in order to avoid inappropriate triggering of intervention pacing.2 consecutive paced60beats at Lower Rate5040Lower Rate30Rate Drop Detection in Medtronic Kappa® Series Pacemakers
118Using Both Detection Algorithms When both detection algorithms are used:Detection occurs when either Drop Detection or Low Rate Detection criteria are metIntervention Rate, Duration and Termination are programmed the same as when using the individual detection modesRate Drop Detection in Medtronic Kappa® Series PacemakersRate Drop Detection with “Both” OptionThe “Both” option works exactly as you would expect it to work:.Intervention occurs when either Drop Detect or Low Rate Detect criteria are met. Each method operates independently.Drop Size and Drop Rate parameters are selected as for Drop Detect.Detection beats is programmed as for Low Rate Detect.Intervention Rate and Duration parameters apply for both detection modes.Intervention works the same as for either individual mode.Termination works the same as for either individual mode.Rate Drop Detection in Medtronic Kappa® Series Pacemakers
119Rate Drop Intervention Therapy DDD or DDI pacingPacing interventionPaces at programmed Intervention Rate for programmed durationPacing terminationPacing rate decreases until there are three consecutive atrial senses or Lower Rate is reachedRate Drop Detection in Medtronic Kappa® Series PacemakersIntervention therapy is available in DDD and DDI modes.Pacing intervention starts at the programmed Intervention Rate and lasts for the programmed Duration. Intervention rates are programmable from bpm. Intervention pacing rates should be set as fast as possible without causing patient discomfort ( bpm), however, intervention should not be programmed less than 90 bpm. If patients are bothered by intervention pacing, this rate can be reduced somewhat.At the end of the Intervention Duration, the pacing rate decreases in steps until there are three consecutive atrial senses or the Lower Rate is reached.Rate Drop Detection in Medtronic Kappa® Series Pacemakers
120Challenges of Syncope Cost Quality of Life Implications Cost/yearCost/diagnosisQuality of Life ImplicationsWork/financialMobility (automobiles)PsychologicalDiagnosis & TreatmentDiagnostic yield and repeatability of testsFrequency and clustering of eventsDifficulty in managing/treating/controlling future eventsAppropriate risk stratificationComplex EtiologySyncope impacts patient quality of life, and health care costs in important ways.Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm (and if possible the arterial pressure) during a spontaneous faint.
121Diagnosing VVS Patient history and physical exam Positive tilt table test (ACC Consensus Protocol)Overnight fastECGBlood pressureSupine and uprightTilt to degreesIsoproterenolRe-tilt60° - 80°Diagnosing VVSVVS is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed, Such supportive evidence may include:Patient history, physical examination, ECG, and other tests provide no diagnosis for patient complaints of syncope.Patient experiences syncope during head-up tilt table testing. Test completion without syncope is a negative result.The following HUT protocol is based on the ACC Consensus Document on tilt table testing (Benditt 1996). Other accepted HUT protocols do exist.Overnight fast, morning testECG (at least 3 leads)Continuous blood pressure monitoringPatient remains supine on the table for minutes.Tilt to degrees for minutes.Lower to horizontal and administer isoproterenol at 1-5 g/min until heart rate increases 25%.Re-tilt for 10 minutesREFERENCE:Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for syncope. ACC Expert Consensus Document. JACC. 1996;28(1):DG Benditt, Tilt Table Testing, 1996.
122VVS: Treatment Overview Educationsymptom recognitionreassurancesituation avoidanceTilt-Trainingprescribed upright posturePharmacologic Agentssalt/volume managementbeta-adrenergic blockersSSRIsvasoconstrictors (e.g., midodrine)Cardiac PacemakersThe treatment of recurrent VVS should focus primarily on education and salt/volume maintenance. Thereafter, physical maneuvers such as tilt-training are recommended. Pharmacologic and pacing treatment options remain for patients who continue to be symptomatic.
123Tilt-Training: Clinical Outcomes 42 HUT positive (21±13 min) VVS patientsHome training: two 30 minute sessions dailyOutcomes41/42 pts --->45 min asymptomatic HUTClinical follow-up: 15.1±7.8 mos36 pts syncope free4 pts: presyncope1 pt: syncope recurrencesThe use of tilt-training has added an important dimension to treatment of recurrent VVS, and may also be of value in some forms of orthostatic hypotension.ADDITIONAL REFERENCES:.Ector H, Reybrouck T, Heidbuchel H, Gewillig M, Van de Werf F. Tilt training: a new treatment for recurrent neurocardiogenic syncope or severe orthostatic intolerance. PACE 1998;21:.Di Girolamo E, Di Iorio C, Leonzio L, Sabatini P, Barsotti A. Usefulness of a tilt training program for prevention of refractory neurocardiogenic syncope in adolescents. A controlled study. Circulation 1999;100:Reybrouck et al. PACE 2000; 23:493-8