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Acute Myocardial Infarction in the Young Presented by Glenn Michael L. Gayos M.D. MAKATI MEDICAL CENTER MEDICAL GRAND ROUNDS.

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Presentation on theme: "Acute Myocardial Infarction in the Young Presented by Glenn Michael L. Gayos M.D. MAKATI MEDICAL CENTER MEDICAL GRAND ROUNDS."— Presentation transcript:

1 Acute Myocardial Infarction in the Young Presented by Glenn Michael L. Gayos M.D. MAKATI MEDICAL CENTER MEDICAL GRAND ROUNDS

2 OBJECTIVES: To present a case of acute myocardial infarction in the young. To present a case of acute myocardial infarction in the young. To discuss the etiology, approach, management to the young patient with myocardial infarction To discuss the etiology, approach, management to the young patient with myocardial infarction

3 GENERAL DATA: W.V. 35 YEAR OLD MALEFILIPINOMARRIED

4 CHIEF COMPLAINT CHEST PAIN

5 HISTORY OF PRESENT ILLNESS: One week PTA (+) CHEST PAIN on the anterior chest well described as heaviness with no radiation (+) Self medicated with Aspirin with relief of sxs Few Hours PTA(+) While watching television, Recurrence of CHEST PAIN on the left anterior chest wall described as heaviness with radiation to the back. Persisting for more than thirty minutes Severity of pain 10/10 (+) Difficulty in breathing

6 PAST MEDICAL HISTORY: CVD May 2008 (2 weeks PTA )with right sided residuals, medications prescribed but not taken CVD May 2008 (2 weeks PTA )with right sided residuals, medications prescribed but not taken (-) DM (-) DM (-) HTN (-) HTN (-) allergies (-) allergies (-) CA (-) CA

7 Family History Family History Hypertension both sides Hypertension both sides (-) DM, (-) Cancer, (-) Thrombosis, (-) early stroke or MI (-) DM, (-) Cancer, (-) Thrombosis, (-) early stroke or MI Personal Social History Personal Social History 25 pack year smoking history 25 pack year smoking history Occasional alcoholic beverage drinker Occasional alcoholic beverage drinker Denies history of drug intake or stimulants Denies history of drug intake or stimulants

8 REVIEW OF SYSTEMS (-) headache, (-) loss of consciousness (-) headache, (-) loss of consciousness (-)easy bruisability (-) rashes (-)easy bruisability (-) rashes (-) easy fatigability, (-) palpitations, (-) easy fatigability, (-) palpitations, (-) abdominal pain (-) diarrhea no constipation (-) abdominal pain (-) diarrhea no constipation (-) edema (-) rashes (-) caudication (-) edema (-) rashes (-) caudication (-) arthralgia, (-) limitation of motion (-) arthralgia, (-) limitation of motion

9 Physical Examination on Admission Bp 130/80 HR 106 RR 24 Temp 37.5 Bp 130/80 HR 106 RR 24 Temp 37.5 W.T. 55 kg H.T. 163cm BMI 20 JVP 8-9 W.T. 55 kg H.T. 163cm BMI 20 JVP 8-9 Conscious coherent in cardio-pulmonary distress Conscious coherent in cardio-pulmonary distress Anicteric sclerae, pink palpebral conjunctivae no carotid bruits no neck vein distention no CLAD Anicteric sclerae, pink palpebral conjunctivae no carotid bruits no neck vein distention no CLAD Equal chest expansion, No retractions, Equal fremitus clear breath sounds Equal chest expansion, No retractions, Equal fremitus clear breath sounds

10 Physical Examination on Admission Adynamic precordium tachycardic regular rhythm no murmurs distinct S1& S2 no S3 noted Adynamic precordium tachycardic regular rhythm no murmurs distinct S1& S2 no S3 noted Flat soft non-tender abdomen Flat soft non-tender abdomen Full and equal pulses no edema no cyanosis Full and equal pulses no edema no cyanosis Neuro-examination =shallow nasolabial fold ®, 5/5 motor function on all extremities no sensory deficit Neuro-examination =shallow nasolabial fold ®, 5/5 motor function on all extremities no sensory deficit

11 SALIENT FEATURES 35 year old male 35 year old male chest tightness of more than 30 minutes duration chest tightness of more than 30 minutes duration Diaphoresis Diaphoresis CVD 2 weeks PTA CVD 2 weeks PTA Smoker 25 pack years Smoker 25 pack years Bp 130/80 HR 106 RR 24 Equal chest expansion Tachycardic Equal Pulses Shallow nasolabial fold R

12 AT THE EMERGENCY ROOM 12 Lead ECG, 12 Lead ECG, 12 Lead ECG 12 Lead ECG Chest x ray, Chest x ray,hest x rayhest x ray serum electrolytes serum electrolytes cardiac enzymes, cardiac enzymes, CBC CBC CBC Urinalysis Urinalysis Urinalysis Nitroglycerine ISDN drip Enoxaparin Morphine ASA/ Clopidogrel 02 via nasal cannula Diazepam

13 WORKING DIAGNOSIS S-T elevation Myocardial Infarction Anterolateral Wall S-T elevation Myocardial Infarction Anterolateral Wall S/P Cerbrovascular Disease S/P Cerbrovascular Disease To consider Hypercoagulable State To consider Hypercoagulable State

14 Admitted under Cardiology Service Admitted under Cardiology Service Immediately Referred Patient to interventional cardiology for Primary PTCA Immediately Referred Patient to interventional cardiology for Primary PTCA Neuro Referral Neuro Referral Recommendations: CT Scan Recommendations: CT Scan CVD Infarct noted CVD Infarct noted CVD

15 REPERFUSION STEMI px presenting to hospital with PCI capability should treat with primary PCI within 90 mins of medical contact STEMI px presenting to hospital with PCI capability should treat with primary PCI within 90 mins of medical contact AHA 2007 STEMI ( MODIFIED Intervention AHA 2007 STEMI ( MODIFIED RECOMMENDATION)CLASS, RECOMMENDATION)CLASS, ASSENT-4 PCI

16 CATH LAB REPORT OF CORONARY ANGIO AND PCI Emergency left heart catherization with coronary angiography and percutaneous coronary intervention/stenting of left main coronary artery were done by percutaneous seldinger technique using 6f Judkins catheters via the right femoral artery with no difficulty or complications Emergency left heart catherization with coronary angiography and percutaneous coronary intervention/stenting of left main coronary artery were done by percutaneous seldinger technique using 6f Judkins catheters via the right femoral artery with no difficulty or complications

17 Coronary Angiography: Totally occluded Left Main Segment

18 CARDIAC CATHETERIZATION REPORT CORONARY ANGIOGRAPHY: Selective cannulation of the LCA with a 6F JL4 catheter shows a TOTALLY OCCLUDED LEFT MAIN SEGMENT. Selective cannulation of the RCA with a 6F JR4 cathter shows a very large and dominant vessel with two large patent posterior descending branches. PROCEDURE: Emergency left heart catheterization with coronary angiography and percutaneous coronary intervention/ stenting of left main coronary artery were done by percutaneous Seldinger technique using 6F Judkins catheter via the right femoral artery with no difficulty or complications. The patient tolerated the procedure well (IABP was on standby). CATHETERS USED: 6 F JL4 AND JR4 Cordis diagnostic catheters 6F XB 3.5 Cordis Vistabrite tip guide catheter CONTRAST USED: 130 ML Ultravist 370

19 PCI A 6F XB 3.5 Cordis Vistabrite tip guiding catheter was used to engage the left main. A 0.014 x 180 cm Cordis Supersoft Stabilitzer wire was used to cross the lesion and positioned into the distal LAD. A 2.0 (15 mm length) Terumo Ryujin rapid exchange balloon was then advanced across the lesion and then inflated at 12 atm for 23 seconds. A second balloon 3.0 x 15 mm Sprinter was used to further dilate the lesion at 12-14 atm for 11-33 seconds. Post balloon angiogram showed a residual stenosis of 40 – 50%. A Taxus 3.5 x 20 mm stent was then advanced across the lesion and deployed at 8 atm for 36 seconds. The delivery balloon was re-inflated at 14 atm for 13 seconds. Post-stent angiogram of the left main LAD showed no significant residual stenosis at the lesion site with TIMI-2 antegrade distal flow, no contrast staining and no loss of side branches. No significant change in the post-stenting angiographic results occurred after an observation period of 5 – 7 minutes. The procedure was terminated with the patient in stable condition.

20 CARDIAC CATHETERIZATION REPORT BALLOON INFLATION Lesion dilated: Left main-proximal LAD SITE Balloon/ Stent SizeDuration(sec)Pressure(atm) Left Main LAD Ryujin balloon 2.0 x 15 mm 2312 Sprinter balloon 3.0 x 15 mm 11331214 Taxus stent 3.5 x 20 mm 368 Delivery balloon 1314

21 PTCA CONCLUSION Successful Primary PCI/stent deployment of the Left Main - LAD Successful Primary PCI/stent deployment of the Left Main - LAD

22 Total Occlusion of Left Main Coronary Artery Rare occurrence with 2.6% frequency in one study Rare occurrence with 2.6% frequency in one study Generally presents as pulmonary edema, cardiogenic shock, or sudden death Generally presents as pulmonary edema, cardiogenic shock, or sudden death PTCA feasible and effective procedure PTCA feasible and effective procedure Effect of Primary Angioplasty on Total or Subtotal Left Main Occlusion Effect of Primary Angioplasty on Total or Subtotal Left Main Occlusion Analysis of Incidence, Clinical Features, Outcomes, and Prognostic Determinants Analysis of Incidence, Clinical Features, Outcomes, and Prognostic Determinants Hon-Kan Yip, MD; Chiung-Jen Wu, MD; Mien-Cheng Chen, MD; Hsueh-Wen Chang, PhD; Kelvin Yuan-Kai Hsieh, MD; Chi-Ling Hang, MD and Morgan Fu, MD Hon-Kan Yip, MD; Chiung-Jen Wu, MD; Mien-Cheng Chen, MD; Hsueh-Wen Chang, PhD; Kelvin Yuan-Kai Hsieh, MD; Chi-Ling Hang, MD and Morgan Fu, MD

23 POST PTCA 30 minutes Post PTCA 30 minutes Post PTCA Patient had episodes of desaturation Patient had episodes of desaturation O2 inhalation increased to fio2 100 % (02 sat 80- 90%) O2 inhalation increased to fio2 100 % (02 sat 80- 90%) Patient intubated Patient intubated Pulmo referral done Pulmo referral done CXR post intubation revealed pulmonary congestion/ pulmonary edema CXR post intubation revealed pulmonary congestion/ pulmonary edema ABG done ABG done ABG

24 CHEST X-RAY (POST INTUBATION) BASELINE CXRAY CXRAY AFTER < 6 HOURS

25 AT THE TELEMETRY Episodes of non-sustained ventricular tachycardia Episodes of non-sustained ventricular tachycardia Patient started on AMIODARONE for Post PTCA arrythmia Patient started on AMIODARONE for Post PTCA arrythmia INITIAL LOADING DOSE (150 mg) INITIAL LOADING DOSE (150 mg) MAINTENANCE DRIP (900 mg x 24 hours) MAINTENANCE DRIP (900 mg x 24 hours) Patient admitted to Telemetry Unit Patient admitted to Telemetry Unit Referral to Nephrology Service for renal prophylaxsis and decreased urine output Referral to Nephrology Service for renal prophylaxsis and decreased urine output CT angiography with renal prophylaxis done CT angiography with renal prophylaxis done D-dimer 642.60 ng/ ml (<500 ng/ ml) D-dimer 642.60 ng/ ml (<500 ng/ ml)

26 2D ECHOCARDIOGRAM (06/03/08) Concentric left ventricular hypertrophy with hypokinetic anterior interventricular septum, anterior and lateral left ventricle from mid to apex. Left ventricular ejection fraction is reduced, 56% (Teicholz) / 52 % (Simpsons). Normal left atrial dimension. Normal right atrial and ventricular dimensions. Normal main pulmonary artery diameter. Normal diameter of aortic root and proximal ascending aorta (2.5 cm). Thickened margins of right and non-coronary cusps of aortic valve leaflets with normal mobility pattern. Normal mitral, tricuspid and pulmonic valves. Color Flow and Doppler study: Mitral regurgitation, mild. Tricuspid regurgitation, mild. Normal pulmonary artery pressure (by pulmonary acceleration time >110 msec). Normal left ventricular diastolic function indices (E/A ratio = 1.3; IVRT = 80 msec)

27 CT ANGIOGRAPHY 6/3/08 6/3/08 Bilateral marked pneumonic consolidation in both lower lobes as well as in the upper lung regions Bilateral marked pneumonic consolidation in both lower lobes as well as in the upper lung regions Normal Ct angiography of the pulmonary vessels including the thoracic aorta Normal Ct angiography of the pulmonary vessels including the thoracic aorta No evident pulmonary embolism No evident pulmonary embolism

28 ECG POST PTCA

29 2020H non-sustained v-tach 2020H non-sustained v-tach Magnesium Sulfate 4 gram in 50ml D5w x 30min Magnesium Sulfate 4 gram in 50ml D5w x 30min Dopamine inotropic support Dopamine inotropic support

30 First Hospital Day Coffee ground/per NGT Enoxaparine discontinued Coffee ground/per NGT Enoxaparine discontinued Repeat Cardiac Enzymes Repeat Cardiac Enzymes Repeat Cardiac Enzymes Repeat Cardiac Enzymes Diagnostic Test Diagnostic Test Diagnostic Test Diagnostic Test Hypercoagulable Work- up Hypercoagulable Work- up Hypercoagulable Work- up Hypercoagulable Work- up Medications Dopamine / Dobutamine Furosemide 40mg Piperacillin Tazobactam Metoprolol Nicorandil

31 ECG on 1 st HD

32 2 nd HD Episodes of hypotension Episodes of hypotension Bilateral Rales (base-mid) Bilateral Rales (base-mid) CXR increased congestion CXR increased congestion Episodes of Chest Pain Episodes of Chest Pain Treatment Dopamine /Dobutamine Furosemide Increased NTG patch transfer of patient to ICU was done.

33 3 rd HD Continuous titration of Dopamine/ Dobutamine Increased Furosemide Correction with KCL Episodes of Hypotension Episodes of Hypotension Persistence of pulmonary congestion Persistence of pulmonary congestion Electrolyte abnormalities Electrolyte abnormalities

34 4 th HD Repeat 2d Echo (6/7/08) Repeat 2d Echo (6/7/08) Concentric left ventricular hypertrophy with segmental wall motion abnormality over left anterior descending artery distribution with preserved global systolic function, EF 59% Concentric left ventricular hypertrophy with segmental wall motion abnormality over left anterior descending artery distribution with preserved global systolic function, EF 59% Dilated aortic root aortic sclerosis, MR moderate, TR mild Dilated aortic root aortic sclerosis, MR moderate, TR mild Improvement of thickening of anterior and lateral wall compared to (6/3/08) Improvement of thickening of anterior and lateral wall compared to (6/3/08)

35 6 th HD Weaning Started via SIMV Weaning Started via SIMV IV amiodarone shifted to Oral IV amiodarone shifted to Oral Tapering of Pressors Started Tapering of Pressors Started CXR showed clearing of pulmonary congestion CXR showed clearing of pulmonary congestion

36 7 th HD Patient extubated Patient extubated NGT removed NGT removed Clear liquid diet with 1.2L/day Clear liquid diet with 1.2L/day Tapering of Dobutamine Started Tapering of Dobutamine Started

37 On the 10 th HD Normal CXR Normal CXR Dobutamine tapered off Dobutamine tapered off Anti-Cardiolipin Results Anti-Cardiolipin Results Anti-Cardiolipin Warfarin 5mg initially Warfarin 2.5mg OD

38 On the 24 th HD Discharged Stable and Improved Discharged Stable and Improved Home Medications Home Medications ASA 80 mg tablet 1 tablet daily Clopidogrel 75 mg tablet 1 tablet daily Nicorandil 10 mg tablet ½ tablet 2x a day Amiodarone 200 mg tablet 1 tablet 2x a day Cilostazol 100 mg tablet 1 tablet 2x a day Metoprolol 50 mg tablet ½ tablet 2x a day Atorvastatin 40 mg tablet 1 tablet once a day Warfarin (Coumadin) 5 mg tablet T – Th 2.5 mg tablet M W F ST SU

39 DISCHARGE DIAGNOSIS: Myocardial Infarction Left Main Segment KILLIP III Myocardial Infarction Left Main Segment KILLIP III Pulmonary Congestion Pulmonary Congestion S/P CVD Lacunar Infarct LMCA (May 2008) S/P CVD Lacunar Infarct LMCA (May 2008) S/P PTCA (6/3/08) S/P PTCA (6/3/08) T/Connective Tissue Disease T/Connective Tissue Disease Anti-phospholipid Antibody Syndrome Suspect Anti-phospholipid Antibody Syndrome Suspect

40 DISCUSSION

41 DEFINITION Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. Detection of rise/fall of cardiac biomarkers Detection of rise/fall of cardiac biomarkers together with evidence of myocardial ischemia together with evidence of myocardial ischemia with at least one with at least one Symptoms of ischemia Symptoms of ischemia ECG changes ECG changes Pathologic Q waves in ECG Pathologic Q waves in ECG Evidence of loss of viable myocardium or wall motion Evidence of loss of viable myocardium or wall motion

42 Epidemiology Myocardial infarction (MI) under the age of 40 years accounts for around 3%-10% of cases of coronary artery disease. Myocardial infarction (MI) under the age of 40 years accounts for around 3%-10% of cases of coronary artery disease. Incidence of MI is approximately 8 times lower in patients 18 to 45 years than in older patients Incidence of MI is approximately 8 times lower in patients 18 to 45 years than in older patients

43 Clinical Presentation -Angina progressing rapidly to fully evolved myocardial infarction -Symptoms present less than 1 week duration -Rarely presents with classic presentation of worsening angina culminating in MI

44 Causes of MI the Young

45 Causes of MI in the Young Cocaine Abuse Cocaine Abuse Atheromatous Coronary Artery Disease Atheromatous Coronary Artery Disease Coronary Artery Dissection/ Aneurysm Coronary Artery Dissection/ Aneurysm Kawasakis, Takayasus Kawasakis, Takayasus Hypercoagulable State Hypercoagulable StateState Anti-phospolipid Antibody Syndrome (primary/secondary) Anti-phospolipid Antibody Syndrome (primary/secondary) Factor V Leiden Factor V Leiden

46 Atheromatous Coronary Artery Disease 80% of acute myocardial infarction in the young 80% of acute myocardial infarction in the young The atheromatous process starts early The atheromatous process starts early CHD was found in 20% of men and 8% of women between the ages of 30 and 34 years of age CHD was found in 20% of men and 8% of women between the ages of 30 and 34 years of age Rom J Intern Med, January 2006 Ginghin et al Rom J Intern Med, January 2006 Ginghin et al

47 Non-Atheromatous Coronary Artery Disease Aortic Dissection Aortic Dissection Aneurysms, ectasia, and anomalous origin of coronary arteries Aneurysms, ectasia, and anomalous origin of coronary arteries Coronary artery aneurysms Coronary artery aneurysms congenital or acquired secondary to Kawasakis disease in childhood congenital or acquired secondary to Kawasakis disease in childhoodK

48 MI with Normal Coronary Arteries Coronary Artery Spasm Coronary Artery Spasm Hypercoagulable States Hypercoagulable States Embolic Phenomena Embolic Phenomena Embolic phenomena Embolic phenomena Paroxidical Phenomena Paroxidical Phenomena 1-12% occurence based on Coronary Angiography Typical patient is young, without any previous history of chest pain Mean age at largest series of MI in patients with normal coronary arteries patients, was 43 years and 43% were women. significantly less frequent angina prior to myocardial infarction. cardiovascular risk profile is lower than that of patients with CAD, Characteristics and Prognosis of Myocardial Infarction in Patients With Normal Coronary Arteries from CHESTPeter Ammann, MD; Sabine Marschall, MD; Martin Kraus, MD; Lucius Schmid, MD; Walter Angehrn, MD; Reto Krapf, MD and Hans Rickli, MD CHEST

49 MI related to substance Abuse Cocaine use is associated with various cardiac complications including MI. Cocaine use is associated with various cardiac complications including MI. 48% of non-traumatic chest pain in the young associated with cocaine use 48% of non-traumatic chest pain in the young associated with cocaine use 6% MI at ER. after various complications after cocaine use. 6% MI at ER. after various complications after cocaine use. Cardiovascular Complications of Cocaine Use Richard A. Lange, M.D., and L. David Hillis, M.D.

50 Hypercoagulable States PRIMARYSECONDARY Antithrombin deficiency Antiphospholipid syndrome Protein C deficiency Factor V Leiden Disorders of the fibrinolytic system Hypoplasminogenemia Hypoplasminogenemia Abnormal plasminogen Abnormal plasminogen Plasminogen activator deficiency Plasminogen activator deficiency Factor XII deficiency Factor XII deficiency Dysfibrinogenemia Dysfibrinogenemia Others: elevation of factor VIII Abnormalities of coagulation and fibrinolysis Trosseau syndrome Trosseau syndrome Nephrotic syndrome Abnormalities of the blood vessels and flow Venous stasis Venous stasisHomocystinuria Thrombotic thrombocytopenic purpura Thrombotic thrombocytopenic purpura Abnormalities of the platelets Myeloproliferative disorders Myeloproliferative disorders Paroxysmal hemoglobinuria Paroxysmal hemoglobinuria Diabetes mellitus Diabetes mellitus

51 Clotting Cascade

52 Factor V Leiden (resistance to APC) Site Venous, occasional arterial, Dx -APC resistance assay aPTT with exogenous APC / aPTT without APC Normal > 2.2 -modified APC-resistance assay. -FV leiden DNA-based analysis by PCR : Loss of principal aPC cleavage site on factor V protein Resistance to inactivation of Factor Va by APC

53 Anti-phospholipid Antibody Syndrome Autoimmune thrombotic disease. Autoimmune thrombotic disease. It is characterized by recurrent arterial or venous thrombosis, recurrent fetal loss or in-utero death and/or thrombocytopenia It is characterized by recurrent arterial or venous thrombosis, recurrent fetal loss or in-utero death and/or thrombocytopenia CVD most frequent thromboembolic manifestations CVD most frequent thromboembolic manifestations MI with normal coronary arteries MI with normal coronary arteries presence of AAS among young patients with AMI ranges from 14% to 21%, presence of AAS among young patients with AMI ranges from 14% to 21%, Rev Clin Esp. 2001; 201(3):118-21 (ISSN: 0014-2565) Seijas M ; Martínez Vázquez C ; Rivera A ; Rayo N ; Ordi-Ros J ; Nodar A ; Picón J

54 DIAGNOSTIC CRITERIA FOR APAS International Consensus Statement on an update of the classification criteria for definite Antiphospholipid Syndrome 2006. Clinical Criteria Laboratory Criteria Vascular thrombosis – one or more episodes of arterial, venous or small vessel thrombosis in any tissue or organ. Vascular thrombosis – one or more episodes of arterial, venous or small vessel thrombosis in any tissue or organ. (confirmed by imaging, Doppler studies or histopathology) Recurrent pregnancy loss. Recurrent pregnancy loss. Anticardiolipin antibody of IgG and/or IgM isotype on two Anticardiolipin antibody of IgG and/or IgM isotype on two occasions at least 12 weeks apart. Lupus anticoagulant in plasma on two occasions at least 12 weeks apart. Lupus anticoagulant in plasma on two occasions at least 12 weeks apart. * Anti b2 glycoprotein I Antibody of IgG or IgM isotype in serum or plasma present on two occasions at least 12 weeks apart

55 ANTIPHOSPHOLIPID ANTIBODY SYNDROME

56

57 ALGORITHMIC APPROACH TO APAS

58 Management of Acute Myocardial Infarction Reperfusion (minimize total ischemic time) Reperfusion (minimize total ischemic time) Restoration of balance between O2 supply and demand Restoration of balance between O2 supply and demand Pain Relief Pain Relief Prevention of Compilations Prevention of Compilations

59 GOLDEN PERIOD

60 MEDICAL MANAGEMENT ANALGESIA- MORPHINE ASPIRIN BETA BLOCKERS BETA BLOCKERS ACE INHIBITORS/ ARB THIENOPYRIDINES

61 REPERFUSION Primary Invasive Strategy Primary Invasive Strategy Goal Door To balloon time 90 minutes Goal Door To balloon time 90 minutes May give >12 hours May give >12 hours Patients with caridogenic shock Patients with caridogenic shock Primary PTCA Primary PTCA Facilitated PTCA Facilitated PTCA Rescue PTCA Rescue PTCA Fibrinolytic Therapy Door to needle time 30minutes May give within 12 hours of onset of symptoms Contraindications Hemorrhage Intracranial mass/stroke AVM Active bleeding 2007 Focused Update of the ACC/AHA

62 SECONDARY PREVENTION CONTROL OF MODIFIABLE RISK FACTORS SMOKING CESSATION SMOKING CESSATION WEIGHT LOSS WEIGHT LOSS EXERCISE EXERCISE Lipid and Sugar Management Lipid and Sugar Management Lipid Anti-coagulation for Hypercoagulable States

63 PROGNOSIS IN THE YOUNG Better outcomes during medium and short term follow-up due to better baseline characteristics but may have higher long term morbidity and mortality Better outcomes during medium and short term follow-up due to better baseline characteristics but may have higher long term morbidity and mortality Greater influence of Modifiable Risk factors towards prognosis Greater influence of Modifiable Risk factors towards prognosis Increased prevalence of smoking, hypertension and obesity in the young Increased prevalence of smoking, hypertension and obesity in the young Acute Myocardial Infarction in Young Adults from American Heart JournalElvis Brscic, MD, et al Acute Myocardial Infarction in Young Adults from American Heart JournalElvis Brscic, MD, et alAmerican Heart JournalAmerican Heart Journal

64 MODIFIABLE RISK FACTORS Observed that smoking, obesity, and hypertension more prevalent in young, high-risk, post-MI patients Observed that smoking, obesity, and hypertension more prevalent in young, high-risk, post-MI patients dyslipidemia and diabetes were less prevalent. dyslipidemia and diabetes were less prevalent. Smoking and hypertension were associated with a differentially increased relative risk of adverse outcomes in younger patients. Smoking and hypertension were associated with a differentially increased relative risk of adverse outcomes in younger patients. need for aggressive efforts at minimizing modifiable risk factors in young patients at risk for and after MI. need for aggressive efforts at minimizing modifiable risk factors in young patients at risk for and after MI. High-risk Myocardial Infarction in the Young: The VALsartan In Acute myocardial iNfarcTion (VALIANT) Trial High-risk Myocardial Infarction in the Young: The VALsartan In Acute myocardial iNfarcTion (VALIANT) Trial

65 APAS TREATMENT 1. PROPHYLAXIS 2. PREVENTION OF FURTHER THROMBOSES OF LARGE VESSELS - Low dose Aspirin 80 mg tablet 1 tablet once a day - Hydroxychoroquine (reported to decrease the titers of APLAS) - According to American College of Chest Physicians Low Molecular Weight Heparin followed by Oral anticoagulants (Warfarin) to maintain INR of at least 2.5 for 12 months or longer

66 RECOMMENDATIONS REPEAT ANTI-Cardiolipin Anti-body testing after 12 weeks REPEAT ANTI-Cardiolipin Anti-body testing after 12 weeks Continue Clopidogrel and ASA for at least 14 days Continue Clopidogrel and ASA for at least 14 days Rheumatology Follow-up Rheumatology Follow-up Ant-coagulation Ant-coagulation

67 Thank You

68 ECGECG on admission ECG

69 CXRCXR On admission CXR

70 Admission COMPLETE BLOOD COUNT HBHCTRBCWBCLYMPHSEGPLT 17.047.96.017.177020286,000 NaKCREAT TROP I TCPKCPKMBCBG 140.03.31.00.064.00.6162.0 PROTIME: 109.9% activity, 0.9 INR PTT: Patient 28.2 (25.1 – 33.9 sec) Control 29.1 seconds Control 29.1 seconds

71 ABGABG POST INTUBATION ABG PO260.3HCO321.6 PH7.46 02 SAT 92 PCO226.4BE-3.6 FIO2100 PEEP MODEAC

72 DAY 2 DAY 2 NaKBUNCREATCPKMBMg 138.03.521.01.21123.21.9 HBHCTRBCWBCSEGLYMPHMONOPLTS 15.1043.105.4222.27781012221,000

73 URINALYSIS COLOR YELLOW YELLOW TRANSPARENCY HAZY HAZY PH7.5 GRAVITY1.01 PROTIEN NEGATIVE NEGATIVE KETONES NITRITES ESTERASE BLOOD3 RBC255 EPITHELIAL1 RBC255 WBC2 BACTERIA1

74 HYPERCOAGULABLE Work up ANTI-CARDIOLIPIN IgG ANTI-CARDIOLIPIN IgG ANTI-CARDIOLIPIN IgM ANTI-CARDIOLIPIN IgM HOMOCYSTIENE12.5(5-15) Protein c 4.59(4.62-4.94) Protein s 17(13.5-24.1)

75 Hypercoagulable Work-Up Work-Up Functional assay for antihrombin III, C, S Functional assay for antihrombin III, C, S Lupus anticoagulant Lupus anticoagulant Plasma homocysteine Plasma homocysteine Antiphospholipid antibodies Antiphospholipid antibodies Clotting assay activated protein C resistance Factor V Leiden Prothrombin gene mutation

76 WORK-UP Anti-Cardiolipin Ig G 3 mpl(<15) Anti-Cardiolipin Ig M 13mpl (<12.5) 6/16/08 ESR43 ANANegative CRPnegative

77 Chest X-ray 6/3/08 normal 6/3/08 normal 6/3/08 (post intubation) prominent pulmonary vasculature with pulmonary congestion E.T. 2 cm above the carina 6/3/08 (post intubation) prominent pulmonary vasculature with pulmonary congestion E.T. 2 cm above the carina 6/5/08 progression of pulmonary congestion, still with pulmonary edema 6/5/08 progression of pulmonary congestion, still with pulmonary edema 6/9/08 complete clearing of pulmonary congestion 6/9/08 complete clearing of pulmonary congestion

78 Diagnostics 6/3/20086/3/20086/4/2008 6/3/20086/3/20086/4/2008 1250H1646H 1250H1646H D-dimer642.6 D-dimer642.6 CPK0.611001123.2 CPK0.611001123.2 cpkmb64186209810 cpkmb64186209810 trop I0 trop I0

79 ALGORITHMIC APPROACH TO APAS

80 ECG 6/3/08 (1030H) ST Elevation Myocardial Infarction anterolateral wall elevation 6/3/08 (1030H) ST Elevation Myocardial Infarction anterolateral wall elevation 6/3/08( 1330H) Acute St Elevation Myocardial Infarction MI 6/3/08( 1330H) Acute St Elevation Myocardial Infarction MI 6/4/08 antero-septal wall myocardial infarction with reciprocal changes in the inferior leads 6/4/08 antero-septal wall myocardial infarction with reciprocal changes in the inferior leads

81 Cardiac disease in the antiphospholipid syndrome: recommendations for treatment. Committee consensus report. Lupus. 2003; 12(7):518-23 (ISSN: 0961-2033) Lockshin M ; Tenedios F ; Petri M ; McCarty G ; Forastiero R ; Krilis S ; Tincani A ; Erkan D ; Khamashta MA ; Shoenfeld Y Hospital for Special Surgery, Barbara Volcker Center for Women and Rheumatic Diseases, New York, NY 10021, USA. LockshinM@hss.edu RECOMMENDATIONS: Valve abnormalities: anticoagulation is recommended for symptomatic patients with valvulopathy. Prophylactic antiplatelet therapy may be appropriate for asymptomatic patients (recommended by 13/17 experts in an independent review). Committee members disagreed whether corticosteroid therapy is helpful, but agree that distinguishing among presumptive valvulitis (valve thickening on echocardiogram), valve deformity and vegetations is important, as treatment implications may differ. Committee members disagreed whether corticosteroid therapy is helpful, but agree that distinguishing among presumptive valvulitis (valve thickening on echocardiogram), valve deformity and vegetations is important, as treatment implications may differ. Occlusive arterial disease (angina, myocardial infarction): the Committee recommends aggressive treatment of all risk factors for atherosclerosis (hypertension, hypercholesterolaemia, smoking) and liberal use of folic acid, B vitamins and cholesterol- lowering drugs (preferably statins). Hydroxychloroquine for cardiac protection in APS patients may be considered. The Committee also recommends warfarin anticoagulation for those who have suffered thrombosis in the absence of atherosclerosis, but recognizes that developing data may support the use of antiplatelet agents instead. Intracardiac thrombi: the Committee recommends intensive warfarin anticoagulation, and consultation with cardiac surgeons when appropriate. Ventricular dysfunction: the Committee recommends intensive warfarin anticoagulation, and consultation with cardiac surgeons when appropriate. Ventricular dysfunction:

82 Summary Summary The objective of this study was to highlight the need for investigation of antiphospholipid (aPL) antibodies in patients presenting with myocardial infarction (MI) and normal coronary arteries at angiography. We present five patients who were found to have had an MI without evidence of atherosclerosis. All had aPL antibodies and thus fulfilled the diagnosis of antiphospholipid syndrome (APS). Who did not have recurrent events on long-term anticoagulation maintaining an international normalised ratio of 3â4. This study suggests that APS is probably a major cause of MI in those with normal coronary arteries at angiography. It is an important diagnosis to make as they do not require anti-atherosclerotic treatment but appear, from this case series, to do well on high-dose warfarin. Further clinical studies are necessary to look at prevalence and best management in these patients. The objective of this study was to highlight the need for investigation of antiphospholipid (aPL) antibodies in patients presenting with myocardial infarction (MI) and normal coronary arteries at angiography. We present five patients who were found to have had an MI without evidence of atherosclerosis. All had aPL antibodies and thus fulfilled the diagnosis of antiphospholipid syndrome (APS). Who did not have recurrent events on long-term anticoagulation maintaining an international normalised ratio of 3â4. This study suggests that APS is probably a major cause of MI in those with normal coronary arteries at angiography. It is an important diagnosis to make as they do not require anti-atherosclerotic treatment but appear, from this case series, to do well on high-dose warfarin. Further clinical studies are necessary to look at prevalence and best management in these patients.

83 CtCt scan Ct 6/3/08 6/3/08 Suggestive lacunar infarct in the left temporo- parietal subcortical area Suggestive lacunar infarct in the left temporo- parietal subcortical area Unremarkable Ct scan examination of the rest of the brain Unremarkable Ct scan examination of the rest of the brain

84 BETA-BLOCKER Oral B-blockers should be given in the first 24 hours IV B-blockers may be given at time of presentation Contraindications 1) signs of heart failure, 1) signs of heart failure, 2) evidence of 2) evidence of a low output state, a low output state, 3) increased risk* for cardiogenic shock, 3) increased risk* for cardiogenic shock, 4) relative contraindications to beta blockade 4) relative contraindications to beta blockade (Level of Evidence: B) 2007 AHA STEMI (MODIFIED RECOMMENDATION) CLASS I

85 Clopidogrel recommended to administer loading dosse of Clopidogrel 300mg recommended to administer loading dosse of Clopidogrel 300mg Clopidogrel 75 mg daily + ASA in STEMI px regardless of whether they undergo reperfusion with fibrinolytic therapy (at least 14 day Long term maintenance therapy with clopidogrel 75mg daily is reasonable for STEMI patient Long term maintenance therapy with clopidogrel 75mg daily is reasonable for STEMI patient

86 Lipid Control Lipid Control HDL >50 in females > 40 in males HDL >50 in females > 40 in males LDL 100> in non diabetics, 70>in diabetics and high risk patients LDL 100> in non diabetics, 70>in diabetics and high risk patients Increase Omega 3 intake Increase Omega 3 intake Promotion of daily physical activity Promotion of daily physical activity High Serum Cholesteryl Ester Transfer Rates and Small High-Density Lipoproteins Are Associated With Young Age in Patients With Acute Myocardial Infarction High Serum Cholesteryl Ester Transfer Rates and Small High-Density Lipoproteins Are Associated With Young Age in Patients With Acute Myocardial Infarction

87 Kawasaki a generalized vasculitis of unknown etiology generalized vasculitis of unknown etiology vasculitis is most severe in medium-sized arteries but can also occur in veins, capillaries, small arterioles, and larger arteries. vasculitis is most severe in medium-sized arteries but can also occur in veins, capillaries, small arterioles, and larger arteries. In severely affected vessels, the media develops inflammation with necrosis of smooth muscle cells. leading to aneurysms. In severely affected vessels, the media develops inflammation with necrosis of smooth muscle cells. leading to aneurysms. Vessel wall becomes narrowed or occluded due to stenosis or a thrombus. Vessel wall becomes narrowed or occluded due to stenosis or a thrombus. Cardiovascular death usually occurs from a MI secondary to thrombosis of a coronary aneurysm or from rupture of a large coronary aneurysm Cardiovascular death usually occurs from a MI secondary to thrombosis of a coronary aneurysm or from rupture of a large coronary aneurysm

88 Takayasus Disease chronic, progressive, inflammatory, occlusive disease of the aorta and its branches chronic, progressive, inflammatory, occlusive disease of the aorta and its branches Takayasu arteritis is heterogeneous. Most patients present with systemic and vascular symptoms; Takayasu arteritis is heterogeneous. Most patients present with systemic and vascular symptoms; Most erythrocyte sedimentation rate is elevated in most erythrocyte sedimentation rate is elevated in most Classification criteria (3 of 6 criteria are necessary), a Age of 40 years or younger at disease onset Claudication of the extremities Decreased pulsation of one or both brachial arteries Difference of at least 10 mm Hg in systolic blood pressure between arms Bruit over one or both subclavian arteries or the abdominal aorta Arteriographic narrowing or occlusion of the entire aorta, its primary branches, or large arteries in the upper or lower extremities

89 6/3/081125.96/4/081073.56/5/08-2536/6/08-3506/7/08-3906/8/09-150 40mg q12 40mg q 6 40mg/o d

90

91 Figure 1. The Clotting Cascade. Coagulation is initiated by the exposure of blood to tissue factor bound to cell membranes. Tissue factor interacts with factor VIIa to convert factor IX to factor IXa and factor X to factor Xa (only the activated forms are shown). Factor IXa converts factor X to factor Xa. Factor Xa generates factor IIa (thrombin) from factor II (prothrombin). Each of these reactions takes place on an activated cell surface. Once factor IIa is generated, it cleaves plasma fibrinogen to generate fibrin. The tissue-factor-pathway inhibitor forms a quaternary structure with tissue factor, factor VIIa, and factor Xa (shown in blue). The thrombomodulin–protein C–protein S pathway (shown in yellow) inactivates factors Va and VIIIa. Antithrombin III inactivates factors XIa, IXa, Xa, and IIa (shown in orange) in a reaction that is accelerated by the presence of heparan sulfate. In the fibrinolytic pathway, tissue- type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA) convert plasminogen to plasmin. Once generated, plasmin proteolytically degrades fibrin (


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