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Heart Attacks: Killers in Disguise!

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Presentation on theme: "Heart Attacks: Killers in Disguise!"— Presentation transcript:

1 Heart Attacks: Killers in Disguise!
[Title slide] W. Frank Peacock, MD, FACEP Vice Chief, Emergency Department The Cleveland Clinic

2 Agenda What is an Acute Coronary Syndrome? (a heart attack)
Why do you care? CAD is the number one killer in Scotland Who gets ACS? What are the symptoms?

3 Agenda When should you go to the hospital?
why you should go to the hospital? How do we diagnosis it? What happens if your diagnosed with it? What can be done to prevent getting this?

4 How does the heart work? Its just a pump, right?

5 Its also a gland Myocardial injury Fall in LV performance
Activation of RAAS, SNS, ET, and others ANP BNP Peripheral vasoconstriction Hemodynamic alterations Myocardial toxicity Slide 10 Left ventricular dysfunction results from myocardial injury. Changes occur in the peripheral circulation that also affect cardiac function and contribute to the symptoms of HF. Vasoconstrictors – those in the sympathetic nervous system and the Renin Angiotensin Aldostrerone (RAA) System, as well as arginine vasopressin and endothelin – become activated to increase afterload and preload by conserving Na+ ions and water. Vasodilators – hormones in the natriuretic peptide system, as well as endothelin – derived relaxing factor and prostaglandins – help to unload the left ventricle and promote natriuretic action. In other words the actions of ANP and BNP counteract the activation of the RAAS and sympathetic nervous system. Remodeling and progressive worsening of LV function Morbidity and mortality Heart failure symptoms

6 Epidemiology of CHD in the US
Single most frequent cause of death 656,000 deaths in 2002 1 of every 5 deaths Incidence Each year, 1.2 million Americans will have a new or recurrent coronary event, and >40% will die as a result 700,000 events will be first attacks; 500,000 will be recurrences Prevalence 13 million Americans have a history of CHD (acute MI, other acute ischemic (coronary) heart disease, angina pectoris, atherosclerotic cardiovascular disease, and all other forms of heart disease) CHD = coronary heart disease; MI = myocardial infarction. American Heart Association. Heart Disease and Stroke Statistics—2005 Update; 2005.

7 Epidemiology of CHD Scotland
Single most frequent cause of death Incidence Prevalence CHD = coronary heart disease; MI = myocardial infarction. American Heart Association. Heart Disease and Stroke Statistics—2005 Update; 2005.

8 Risk for CHD Increases With Additional Risk Factors: INTERHEART Study
512 256 128 64 32 16 8 4 2 1 Odds ratio (99% Cl) Smk (1) DM (2) HTN (3) ApoB/A1 (4) 1+2+3 All 4 +Obes +PS All RFs PS = psychosocial Yusuf S, et al. Lancet. 2004;364:

9 Odds Ratio for 1st MI (99% CI)
INTERHEART: Impact on CV Risk of Multiple Risk Factors (Smoking, Lipids, Hypertension, Diabetes, Abdominal Obesity, Diet, ↓Physical Activity, Alcohol, Psychosocial*) 512 – Large int’l case-control study – 15,152 cases – 14,820 controls – 52 countries – Follow-up: 4 years 256 128 64 32 Odds Ratio for 1st MI (99% CI) 16 Smk = smoking DM = diabetes HTN = hypertension Obes = abdominal obesity Ps = psychosocial factors 8 4 Design Large international case-control study Participants 15,152 cases; 14,820 controls; 52 countries Objective To determine association of first MI with: Smoking Lipids Hypertension Diabetes Abdom.Obes. Diet Physical Alcohol Psychosocial activity consumption factors (eg, stress, depression) Follow-up 4 years, February 1999–March 2003 Clinical Implications 9 simple and modifiable risk factors are strongly associated with acute MI worldwide • These 9 risk factors account for >90% of the population attributable risk globally and in most regions • Implementing preventive strategies based on our current knowledge would prevent the majority of premature CHD worldwide 2 1 Smk (1) DM (2) HTN (3) ApoB- ApoA1 (4) 1+2+3 All 4 All 4 + Obes All 4 + Ps All risk factors *eg, stress, depression Note: odds ratio plotted on a doubling scale. . Yusuf S, et al. Lancet. 2004;364: Yusuf S, Hawken S, Ounpuu S, et al. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet. 2005;366:

10 What does an ACS feel like?

11 Symptoms of CAD NONE…….. Sudden Cardiac Death Chest Pain
Usually a pressure Not seconds Anginal equivalents Jaw or shoulder pain Nausea & vomiting Shortness of breath Weak & dizzy Diaphoresis

12 Symptoms of Heart Attack
Anginal equivalents Jaw/shoulder pain Nausea & vomiting Shortness of breath Weak & dizzy Diaphoresis Classic presentation Chest pressure Elephant Sweating Nausea/vomiting Radiation of pain Shortness of breath

13 Who gets “Equivalents”?
Women Diabetics Elderly Heart Transplant patients Patients who can’t perceive/communicate well? Drunk Mentally ill

14 Options for Transport of Patients With STEMI and Initial Reperfusion Treatment
Hospital fibrinolysis: door-to-needle within 30 min Not PCI capable Call 9-1-1 Call fast EMS on-scene Encourage 12-lead ECGs Consider prehospital fibrinolytic if capable and EMS-to-needle within 30 min Onset of symptoms of STEMI 9-1-1 EMS dispatch EMS triage plan Inter-hospital transfer PCI capable GOALS 5 min 8 min EMS Transport Patient EMS Prehospital fibrinolysis EMS-to-needle within 30 min EMS transport EMS-to-balloon within 90 min Patient self-transport Hospital door-to-balloon within 90 min This slide summarizes the essential concept of a triage plan for patients with chest pain and underscores the importance of time-to-treatment. Effective treatment delivered within the “Golden Hour” following symptom onset and reducing the total ischemic time to less than 2 hours preserves myocardium and is associated with reduced mortality. For patients with STEMI, reperfusion may be accomplished by fibrinolysis or primary angioplasty. The choice of specific strategy depends on how the patient is being transported and the capabilities of the receiving hospital. The objective is to keep the total ischemic time to 120 minutes or less: Prehospital fibrinolysis should be started within 30 minutes of the arrival of EMS if EMS has fibrinolytic capability and the patient meets the criteria for fibrinolysis; Door-to-needle time should be 30 minutes or less for patients who are fibrinolysis candidates when EMS does not have fibrinolytic capability; Door-to-balloon time should be 90 minutes or less when fibrinolysis is not an option and transport to a PCI-capable hospital is an option. . Dispatch 1 min Golden hr = 1st 60 min Total ischemic time: within 120 min Adapted with permission from Antman EM, et al. Available at: Accessed November 1, 2005. Antman EM, Anbe DT, Armstrong PW, et al, American College of Cardiology, American Heart Association, Canadian Cardiovascular Society. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction—executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004;44:

15 What happens in the Ambulance?
Paramedics take your history and perform a brief exam IV Oxygen Put on the monitor May receive nitroglycerin under the tongue. (tingle, get a H/A) Maybe: ECG, thrombolytic (clot dissolver)

16 What happens when you get to the hospital?

17 ED Visits - US 130,000,000 annually 10.4 M chest pain (8.0%) 6.24 M
suspected or actual cardiac 4.1 M sent home non-cardiac 50,000 MIs 3.1 M non-cardiac (50%) 1.2 M AMI (20%) 1.5 M UA (24%) 374,400 sudden death (6%)

18 Spectrum of Acute Coronary Syndromes
Presentation Ischemic Discomfort at Rest No ST-segment Elevation ST-segment Elevation Emergency Department Cardiac Markers + + + In-hospital 6-24 hours Unstable Angina (UA) Non-Q-wave MI (NSTEMI) Q-wave MI (STEMI) Adapted from Braunwald E, et al. Available at:

19 STEMI: Brief Physical Exam in the Emergency Department
Airway, Breathing, Circulation (ABC) Vital signs, general observation Presence or absence of jugular venous distension Pulmonary auscultation for rales Cardiac auscultation for murmurs or gallops Presence or absence of stroke Presence or absence of pulses Presence or absence of systemic hypoperfusion (cool, clammy, pale/ashen) Antman EM, et al. Available at: Accessed November 1, 2005.

20 STEMI: Acute Medical Therapy
General treatment measures Analgesics Nitrates Oxygen β-blockers (decrease heart rate) Primary PCI or coronary thrombolysis (primary PCI preferred after 3 hours) Aspirin ( mg, acute dose) Heparin If PCI: – Clopidogrel – GP IIb/IIIa inhibitors Infarct size limitation Reperfusion Antithrombotic and antiplatelet therapy Antman EM, et al. Available at: Accessed November 1, 2005.

21 Chest Pain on a Saturday morning
While the physician was examining the ECG, the patient became unconscious and the rhythm on the monitor changed…

22 Chest Pain on a Saturday morning
12:01 100J DC cardioversion, patient immediately in NSR 12:03 Clot box brought to room and catheterization lab team notified 12:04 IV line started, 325 mg aspirin chewed and metoprolol given 12:10 Open cath table and staff available, heparin iv and clopidogrel po given 12:19 Patient’s stretcher rolls

23 Goals of Reperfusion Therapy
Patient Transport In-hospital Reperfusion D-N ≤ 30 min 5 min < 30 min D-B ≤ 90 min Methods of Speeding Time to Reperfusion Media campaign Patient education Greater use of 9-1-1 MI protocol Critical pathway Quality improvement program Bolus lytics Dedicated PCI team Prehospital ECG and Prehospital Rx, if possible Adapted with permission from: Antman EM, et al. Available at: Accessed November 1, 2005.

24 Time from Symptom Onset to Treatment Predicts 1 Year Mortality—Primary PCI
The relative risk of 1 year mortality increases by 7.5% for each 30 minute delay. Roughly 1% every 3 minutes Y=2.86 (± 1.45) X X2 P<.001 De Luca G, et al. Circulation. 2004;109:

25 Meta-analysis of 50,246 Patients in Lytic Trials (Juice to squeeze)
per 1000 treated patients Absolute benefit 20 40 60 80 3 6 9 12 15 18 21 24 Time to Treatment Boersma E, et al. Lancet.1996;348:771

26 Primary PCI vs Thrombolysis in STEMI: Meta-analysis (23 RCTs, N=7739)
25 Short-term Outcomes (4-6 weeks) P<.0001 Bonferroni correction 6 variables: p <0.0083 20 P<.0001 15 P=.0002 P<.0001 Frequency (%) PCI P=.032 10 Thrombolytic therapy 5 P<.0001 This meta-analysis encompassed 23 trials in which 3872 patients with STEMI were randomized to primary percutaneous transluminal coronary angioplasty (PTCA) and 3867 patients were randomized to thrombolytic therapy. Stents were used in 12 of the 23 trials and in 8 trials GP IIb/IIIa inhibitors were used. Results indicated that the incidence of every short-term clinical outcome of interest was significantly higher in patients receiving thrombolytic agents than it was in those who underwent primary PTCA. Results with PTCA continued to be superior to those with thrombolysis during long-term follow-up and were independent of the type of thrombolytic agent used (76% received a fibrin-specific agent rather than streptokinase) and whether or not the patient was transferred to primary PTCA. Death Nonfatal MI Recurrent Ischemia Hemor- rhagic Stroke Major Bleed Death, Nonfatal Reinfarction, or Stroke Adapted with permission from Keeley EC, et al. Lancet. 2003;361:13-20. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003;361:13-20.

27 What if the ECG is not diagnostic?
(As it is in >95%)

28 Blood Markers Necrosis Something has to die Strain
Natriuretic peptides Other Inflammation Plaque rupture Ischemia changes the blood

29 ACS Sequence and Timing
All Ischemia Some Ischemia, Some Necrosis All Necrosis Plaque Rupture Onset of Pain ED Presentation Discharge -12 to 0 hrs 12 to 24 hrs Amount of Tissue Time IMA cTn Ischemia Muscle death Ventricular Overload BNP <> means click the mouse to advance to next in animation We start with a time line of events in an ACS presentation <> A plaque ruptures, which leads to chest pain, which provokes a patient to present to the hospital emergency room, and we label presentation as time zero <> Looking at the amount of tissue involved <>, we can see that the tissue starts ischemic, and prolonged ischemia leads to necrosis, or infarct. <> IMA rises rapidly with the onset of ischemia, and we believe starts to fall as more of the muscle converts from ischemic to necrotic <> Troponin, on the other hand, starts to rise slowly with the onset of necrosis, peaks at about 24 hours after presentation (6 hours or so after all the tissue is necrotic and no more is ischemia), and falls slowly over several days. <> BNP rises once the remaining healthy muscle is required to compensate for the lost pump function of the heart, and therefore may be elevated at the time of discharge. <> Therefore, there is a progression from ischemia (IMA), to necrosis (troponin) to muscle overload (BNP). These three markers together reveal what is happening during the ACS event. BNP

30 Appearance of necrosis markers
10 20 30 40 50 60 70 80 2 4 6 8 12 18 24 32 48 72 Hours After Onset of MI CKMB Myoglobin TnI Hospital arrival Established release kinetics of necrosis markers have consistently demonstrated the sequential release of myoglobin, CKMB and Troponin, respectively. The early rise of myoglobin is also met with an early decline (within 12 hours), making this an important, dynamic surveillance marker in the initial hours post event. It’s dynamic nature also documents the potential value of rapid sequential testing of myoglobin as a way of confirming an acute event vs a pre-existing non cardiac necrotic source. CKMB has greater specificity, is a standardized and trusted immunoassay, and is released within a few hours post AMI. Finally, cardiac Troponin is a highly specific marker but lacks good sensitivity in the first few hours post event. It is clear that these markers complement each other in providing early sensitivity Myoglobin/CKMB with better specificity Troponin I & T. Studies have examined the potential role of using these markers in a panel approach vs any single marker in isolation.

31 Disease vs Events? Oxygen supply diminishes with disease progression
Time Oxygen Oxygen supply diminishes with disease progression Oxygen demand changes daily and during life Ischemia occurs when O2 demand exceeds supply

32 What is in the future? New better markers

33 What is IMA? Human Serum Albumin (HSA) is a circulating protein in blood with a metal binding site at the N-terminus. The N-terminus is altered during an ischemic event, resulting in Ischemia Modified Albumin (IMA™). IMA is unable to bind metals at the N-terminus. Ischemia Modified Albumin = IMA HSA is the most common protein in blood. There is a metal binding site at the N-terminus of IMA – for transition metals copper, cobalt and nickel. It was discovered that exposure to ischemic tissue alters the end terminus of HSA in such a way that it can no longer bind metals. The conversion of HSA to IMA is mediated by free radical production (see later slides). The organ specificity (ie: to myocardial ischemia) is not well understood. Bar Or et al, European Journal of Biochemistry, 2001

34 Chest Pain at Presentation
12% ACS 13% Rule Out 75% Grey Zone Current EP Protocol EP Protocol with good NPV ischemia marker 25% ACS 35% Rule Out 40% Grey Zone Without IMA, the chest pain challenge is what to do with 75% of chest pain patients for whom a diagnosis can not be made at presentation, and therefore are subjected to serial blood draws, and other time consuming and expensive procedures such as provocative testing, myocardial perfusion imaging, echocardiography, angiography, and so on. With IMA, the number of patients who can be discharged early is almost three times as many (the test presently only has indications for use as a rule out). The potential value of a positive IMA test is to expedite diagnostic evaluation or suggesting more rapid or intensive therapy in higher risk patients. Therefore number of patients in the “Grey Zone” is considerably reduced. Excellent clinical data exists to show the value of IMA as a rule out, and additional clinical studies are under way to investigate the value of IMA as a rule in.

35 What if the markers are all negative?
(And they are in >90%)

36 If It Moves, Even Below Your Hospital’s Cutpoint, It Is Bad
Marker Comparator OR for 30 day MACE 95% CI ing Tn vs. stable Troponin 2.25 ing Tn 3.04 ing CKMB vs. stable CKMB 0.67 ing CKMB 0.96 Logistic regression models showing the odds ratios for predicting ACS MACE: MI, revascularization (PCI or CABG), or positive testing (>70% stenosis at catheterization, [+] MPI or non-invasive stress testing) within 30 days of index visit.

37 All this testing… What’s the end result?
Most (88%) of the time, its negative You go home 18% of the time, something is positive ECG  IMMEDIATE Cath lab Marker  URGENT Cath lab Stress test  Semi-elective Cath lab

38 What happens in the Cath Lab?
Define the anatomy Acutely closed vessel  fix it Chronically closed vessel  nothing Stenotic vessel: have options ~50%; either medicine or angioplasty works >70%; most get angioplasty

39 Scotland Epidemiology

40 Prevalence of coronary heart disease in Scotland: Scottish Heart Health Study.
10,359 men and women aged years from 22 districts in the Scottish Heart Health Study Described the prevalence rates of coronary heart disease in Scotland in and their relation to the geographical variation in mortality in these districts. Coronary heart disease in Scotland was the highest reported to the WHO from Angina was more common in men (5.5%) than in women (3.9%) A history of MI was 3 times more common in men than women Angina correlated well with mortality from coronary heart disease Br Heart J Nov;64(5):295-8

41 2001: The good news The Cardiovascular Epidemiology Unit at the University of Dundee celebrated its 20th anniversary with a 40 % decline in coronary mortality rate The steep decline in coronary mortality in Scotland mirrors the pattern in the rest of Britain. Improvement is a combination of: Heightened awareness of health issues Improved diet and more exercise Improvement in treatments. Scotland's record on heart disease is much improved Russia now has the highest coronary mortality rate.

42 2003 British Women's Heart and Health Study
20% MI, angina, HF, CVA, PVD. 50% HTN, 12% smoked, 25% obese 50% w/ total cholesterol > 6.5 mmol/l, only 3% had low HDL Age adjusted CVD prevalence highest in Scotland: 25.0% (21.5% to 28.8%) lowest in S. England: 15.4% (13.5% to 17.6%). Woman in Scotland are 1.53 times more likely to have CVD Of women with CVD 12% are smokers, 1/3 had uncontrolled HTN, 1/3 were obese 90% had a cholesterol > 5 mmol/l. Only 41% were taking antiplatelet drugs and 22% were taking a statin. Journal of Epidemiology and Community Health 2003;57:

43 In Scotland Coronary Heart Disease one of the leading causes of death
10,331 deaths in 2005 Scotland has one of the highest death rates from CHD in the western world Due to high rates of smoking poor diet deprivation

44 In the year ending March 31 2006
Scottish hospitals 48,962 hospital discharges for CHD 16,320 were for AMI(heart attack) CHD discharges represented around 4% of all acute hospital discharges. NHSScotland carried out 2,319 Coronary Artery Bypass Grafts 5,803 angioplasties 17,065 angiographies

45 http://www.isdscotland CHD mortality is strongly related to age.
0-44 year olds is 4.1 per 100,000 75+, the rate is  per 100,000 The incidence of CHD is higher in men, elderly and deprived areas of Scotland Smoking being overweight raised blood pressure raised level of cholesterol

46 Cost of Cardiovascular Disease in the UK
CVD cost the UK £29.1 billion in 2004 (exceeds the GDP of Kuwait) 29% (£8.5 billion) was due to Coronary Heart Disease 27% (£8.0 billion) Cerebrovascular Disease CVD Cost break down 60% health care 23% productivity losses 17% informal care-related costs Conclusions: CVD is a leading public health problem in the UK measured by the economic burden of disease. Heart 2006;92:

47 Small changes in UK cardiovascular risk factors could halve CHD mortality
The UK called for a 40% reduction in CVD mortality by 2010. Potential reductions from the year 2000, were calculated for: Continuation of recent risk factor trends ~10,685 fewer CAD deaths in 2010 than in 2000 Modest additional reductions in cholesterol and smoking ~51,270 fewer deaths Optimistic changes in obesity, DM, and physical activity, would have relatively small effects. Journal of Clinical Epidemiology 58 (2005) 733–740

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