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A. Epidemiology of MI and Coronary Artery Disease (CAD)

  1. Prevalence: ~14 million persons in USA with CAD
  2. MI Incidence: 1.5 million MI per year in USA
  3. About 200,000 deaths from MI per year in USA
  4. About 50% of adults in USA have elevated cholesterol (chol) levels
  5. Cardiovascular disease (CVD, mainly MI and stroke) accounts for nearly 50% of deaths in USA
  6. Major Risk Factors [1,7]
    1. Majority (>80%) of patients with CVD have one of major CAD risk factors:
    2. Cigarette smoking
    3. Diabetes mellitus (DM) [52]
    4. Hyperlipidemia
    5. Hypertension (HTN)
    6. Unclear what additional prognostic information available with emerging risk factors [74]

B. Summary of Risk Factors For MI

  1. Clinical
    1. Previous MI
    2. HTN (even if treated)
    3. Insulin Resistance Syndromes (IRS): DM, Metabolic Syndrome
    4. Smoking ~3X risk increase in acute MI [38]
    5. Male age >45 or Female postmenopausal (age >55 years)
    6. Sedentary Lifestyle
    7. Left Ventricular Hypertrophy (LVH)
    8. Obesity (visceral)
    9. Family History of coronary disease - <55 years for men, <65 years
    10. Sleep Apnea
    11. Cocaine abuse
    12. Hypothyroidism - overt but not subclinical disease is clearly a risk factor [23]
    13. Chronic renal insufficiency, renal failure and dialysis [4,35]
    14. Psoriasis - particularly severe and in young persons [33]
    15. South Asians at increased risk over Chinese and Europeans [5]
    16. Lack of any alcohol consumption is a risk factor
    17. Abdominal aortic aneurysm 3cm or greater (in >64 year olds) [6]
  2. Laboratory
    1. Elevevated low density lipoprotein (LDL) chol
    2. Reduced high density lipoprotein (HDL) chol: <35mg/dL
    3. Hypercholesterolemia - elevated total chol: >200mg/dL (probably related to LDL, Apo B)
    4. Elevated C-reactive protein (CRP) - marker for inflammation, cardiac risk [8,9,13,36,92,95]
    5. Normal CRP <1mg/L; moderate risk 1-3mg/L; high risk >3mg/L [111]
    6. Elevated CRP and high total to HDL chol ratio are most important independent risk factors for systemic atherosclerosis [8,10,92,113]
    7. Elevated B-type natriuretic peptide - 1.2-1.4X increased risk [34,36]
    8. Urinary albumin to creatinine ratio - 1.2X increased risk [34]
    9. Elevated serum homocysteine (HC, levels >10nmol/L) - 1.2X risk [34]
    10. Hemoglobin A1c (HbA1c) levels correlate with risk with or without DM [28,29]
    11. Increased Apolipoprotein B and ApoB/ApoA1 ratio [17,88]
    12. Anti-cardiolipin antibodies (in patients with systemic lupus)
    13. Subclinical hypothyroidism is a ~2X risk factor for MI in women >60 [12]
    14. In patients with low LDL and intermediate CRP, elevated Lp-PLA2 (lipoprotein associated phospholipase A2), is a risk factor [19,75]
    15. Cardiac troponin T and C-reactive protein levels predict cardiac prognosis in hemodialysis patients [107]
  3. Uppsala Longitudinal Study of Adult Men (ULSAM) [36]
    1. Study of biomarkers to predict >10 year CV morbidity and mortality in adult men
    2. Combination of biomarkers more accurate than any one alone in predicting clinical outcomes
    3. Adult men with or without pre-existing cardiovascular disease
    4. Four independent markers were validated:
    5. Troponin I - myocardial damage
    6. N-terminal pro-brain ntatriuetic peptide (NT pro-BNP) - left ventricular dysfunction
    7. Cystatin C - renal dysfunction
    8. C-reactive protein (CRP) - inflammation
    9. These markers were all independent of known, existing CV risk factors
  4. Experimental and Emerging [7,54]
    1. Small, dense LDL particle size [17]
    2. Subtype 3 of HDL [19]
    3. Serum Lp(a) >26mg/dL [16]
    4. Increased Apolipoprotein A1 (ApoA1) may be protective [88]
    5. In a direct comparison study, ratio of apolipoprotein B100 (ApoB) to ApoA1 was a better predictor of myocardial infarction (MI) than any cholesterol ratio [114]
    6. Apolipoprotein E: Genotype 4 (ApoE4) 1.4X, Genotype 2 0.8X risk versus Apo E3 [14,112]
    7. Elevated IL6 (induces CRP production) levels [86,95]
    8. Elevated fasting insulin levels [17]
    9. Elevated serum urate levels [20]
    10. Elevated levels of Factor VII, Factor VIII, and von Willebrand Factor
    11. Coagulation Factor V "Leiden" (1691A) ~1.2X and Prothrombin 20210A ~1.3X CAD risk [21]
    12. Fibrinogen Elevation
    13. Elevated N-terminal pro-Brain (B) natriuretic peptide (BNP) [39]
    14. Serum macrophage inhibitory cytokine 1 (MIC-1) [94]
    15. Estrogen receptor alpha CC genotype (3X MI risk versus CT or TT) [108]
    16. Higher estrogen levels in men associated with reduced CV risk [30]
    17. Elevated Troponin I or T levels [9,107]
    18. Elevated serum myeloperoxidase (MPO) levels [15,87]
    19. Asymmetric dimethylarginine (endogenous nitric oxide synthetase inhibitor) [89]
    20. Reduced levels of albumin and increased leukocyte counts
    21. Aortic sclerosis (in elderly)
    22. Increased carotid arterial intima-media thickness
    23. Combinations of polymorphisms connexin 37, PAI-1, stromelysin polymorphisms [104]
    24. Strong inverse relationship between a patient's red blood cell glutathione peroxidase levels and risk of subsequent CVD events [109]
    25. Paraoxonase 1 (PON1) levels and polymorphisms associated with 1.5-3.5X risks for major cardiac events and and all-cause mortality [55]
  5. Use of emerging risk factors in prognostic assessment not clear [34,74] except for MPO [15]
  6. Adding biomarkers to standard risk factors does not significantly improve prognostic yield [34]

C. Defined Risk Factors for MI [1]

  1. Highest risk for MI is previous MI or other atheroembolic event
  2. DM and IRS
    1. IRS leads to deleterious lipid profile, accelerated atherosclerosis, elevation of systemic inflammation markers in serum
    2. DM risk for first MI is as high as non-DM patients with one MI's risk for second MI
    3. IRS have 2.5-4X increased risk of CV death [17,102]
    4. Elevated HbA1c levels associated with increased CV events with or without DM [28,29]
  3. Smoking [38]
    1. Responsible for ~21% of all mortality from heart disease
    2. Direct smoking causes 2.95X increased risk of MI
    3. Passive smoking increases risk of MI ~15%
    4. Increases levels of CRP, fibrinogen, HC; all risk factors for vascular disease [72]
    5. Quitting within 5 years decreased risk 50-70%
    6. Quitting for 3 years reduced overall MI risk to 1.87X never-smokers
    7. Exercise reduces risk of CVD death by ~35% in smokers
    8. Smoking + Oral Contraceptives: ~39X increased risk
  4. HTN
    1. Systolic blood pressure (BP) is better predictor of coronary risk than diastolic BP [91]
    2. HTN is synergistic with diabetes and elevated chol for CAD
    3. HTN also major risk for stroke
    4. ß-Blocker use associated with reduced risk for MI [25]
    5. However, risks of elevated blood pressures is dependent on age and comorbid conditions, and likely has a threshold component [27]
  5. Lipid Profile
    1. Total chol level >200mg/dL is usual threshhold for initiation of treatment
    2. 2-3% decrease in risk for each 1% decrease in serum chol
    3. The LDL:HDL or total chol:HDL ratios are the good predictors of CAD
    4. ApoB/ApoA ratio may be best overall predictor of CAD [17]
    5. Low HDL (<35mg/dL) is independent risk factor (mainly low HDL-3)
    6. Hypertriglyceridemia is a risk factor mainly in men with high LDL:HDL ratio
    7. High lipoprotein a {Lp(a)} level is a risk factor in middle-aged men [16]
    8. Small diameter LDL particles is associated with CAD but is relatively weak
    9. Statin use associated with reduced risk of MI [25]
  6. Elevated C-reactive protein (CRP) [8,9,10,13]
    1. CRP is an IL6-driven gene expressed in liver
    2. CRP binds to C-protein from streptococci and helps initiate inflammatory response
    3. CRP is a general marker for inflammation
    4. CRP may bind to oxidized LDL and trigger complement activation and inflammation
    5. CRP is the strongest independent nonlipid predictor of systemic atherosclerosis [10]
    6. CRP is predictive of cardiac and overall death (but not cancer risk) in women [92]
    7. CRP polymorphisms associated with elevated CRP levels and atherosclerosis [2]
    8. Soluble adhesion molecules (ICAM, VCAM, P- and E-selectins) levels do not provide risk information beyond CRP and other risk factors [42]
    9. Statins reduce CRP levels and risk of acute cardiac events even with normal lipids [43]
    10. Long term excercise reduces atherogenic activity of mononuclear cells [55]
  7. Obesity [102]
    1. Elevated BMI is a 3-5X risk factor for CAD in both men and women
    2. Abdominal ("apple") obesity is more of a risk factor for CAD than hip ("pear") obesity
    3. Abdominal obesity is a risk factor independent of BMI
    4. Thus, increased waist to hip ratio is an independent risk factor
    5. Strongly associated with metabolic syndrome (IRS)
  8. Exertion Related MI
    1. Usually occur in habitually inactive people with multiple cardiac risk factors
    2. More common in men, smokers and with elevated cholesterol
    3. Risk for MI during exertion in these people is ~10X higher than without exertion
    4. Large thrombus found in infarcted artery
    5. Single vessel disease found in 50% of exertion-associated MIs, versus 28% non-exertion
    6. Strongly recommend risk-factor modification and exercise training in these persons prior to embarking on vigorous physical activities
  9. Left Ventricular Hypertrophy (LVH)
    1. LVH is an independent risk factor for MI and premature death
    2. LVH as a risk is independent of CAD
    3. Reduction of LVH during anti-HTN therapy is independently associated with improved CVD outcomes [11,60]
  10. Elevated Serum HC [34,40]
    1. Elevated HC levels associated with ~10% increase in risk for CAD [101]
    2. Most cases of elevated HC due to medical conditions, drugs or vitamin deficiency
    3. Rare monogenic enzyme deficiencies lead to hereditary form of the disease
    4. About 20% of pateints with hereditary cystathionine ß-synthase deficiency (leading to highly elevated HC) will have a thromboembolic event by age 20
    5. HC enzyme MTHFR 677C±>T polymorphism associated with 1.16X increased risk of ischemic heart disease in patients with reduced folate levels [100]
    6. Unclear if elevated HC is cause, effect, or unrelated to vascular disease
    7. To date, no clear data that reducing HC leads to reduced vascular events [40,85]
  11. Sleep-Related Breathing Disorders increase MI risk ~5.5X [44]
  12. Hypothyroidism - overt and probably subclinical disease
  13. Generalized Atherosclerosis
    1. Assessed by noninvasive B-mode ultrasonography on distal carotid arteries
    2. The majority of cardiac risk factors will also increase carotid atherosclerosis
  14. Cocaine Abuse [45]
    1. Blocks reuptake of norepinephrine, dopamine, and epinephrine
    2. Potent adrenergic activation with marked cardiac and systemic vasoconstriction
    3. Increases inotropy and heart rate, with great increases in cardiac oxygen demand
    4. Synergistic with smoking to cause ischemia and myocardial infarctions
    5. Synergistic with alcohol abuse to cause myocardial damage
  15. Renal Failure [35]
    1. Yearly mortality for hemodialysis patients is 20-25%
    2. Over 50% of deaths are due to CVD causes
    3. HTN is a major risk factor for early CVD death in dialysis patients
    4. Survival after acute MI with dialysis is 40% at 1 year, 10% 5 years
    5. Albuminuria of any level in nondiabetic patients is also a risk for MI and/or death [22,34]
    6. Glomerular filtration rate <60mL/min per 1.73m2 is a ~2X risk for cardiac events [35]
  16. Genetic
    1. Family History - likely underlying, low penetrance genetic predispositions
    2. Male Sex or female sex after menopause - likely related to lipid profiles
    3. Other genetic disease (hyperlipidemias, homocystinuria, thrombotic disorders, others)
    4. Specific mutations in coagulation and coagulation inhibitor proteins
    5. Genetic risk factors for acute coronary syndromes (ACS) have not been validated [3]
  17. Rofecoxib (Vioxx®) has a 1.7-2.4X risk for serious heart disease or MI [24,97,110]
  18. Risk Factors for CAD in Young Persons (<45 years) [48]
    1. Very premature atherosclerosis accounts for ~80% of MIs in persons <45 years
    2. Standard risk factors are major contributors to premature CAD [49]
    3. Endocarditis
    4. Patent foramen ovale
    5. Migraine with (but not without) aura ~2X risk [31]
    6. Oral contraceptive use
    7. Systemic lupus erythematosus (usually with antiphospholipid antibodies)
    8. Congenital coronary artery anomalies
    9. Cocaine abuse (coronary artery spasm)
    10. Blunt chest trauma
    11. Vasculitis
    12. Myocardial oxygen supply / demand imblance (shock, accident, vigorous exercise)
    13. Very strong family history
    14. Protease inhibitors for HIV infection associated with 16% annual increased MI risk [50]

D. Novel Markers for Ischemic Heart Disease Risk

  1. Lipid Metabolism [17]
    1. Apo B (component of LDL and VLDL), small LDL particles and insulin levels
    2. Elevations in these three risk factors increases risk of ischemic heart diseases ~18 fold
    3. These markers represent more biologically relevant molecules than standard tests
    4. Hypertriglyceridemia itself may be a risk factor for CAD; this is still unclear
    5. Lipoprotein(a) excess may be a risk factor for CAD; data remain equivocal
  2. Lipoprotein Associated Phospholipase A2 (LP-PLA2) [19]
    1. Circulates in blood with both LDL and HDL, and levels correlate with LDL levels
    2. LP-PLA2 degrades the proinflammatory cytokine PAF (and other lipids)
    3. Unclear if LP-PLA2 is pro- or anti-inflammatory
    4. LP-PLA2 level is a strong, independent risk factor for MI in a large study [19]
  3. Clotting Pathway Variants
    1. Mutations in clotting pathway genes can predispose to thromboembolic disease
    2. Deficiency in protein S, C, or antithrombin increases risk
    3. Factor V Leiden and Factor VII [53] mutations may increase risk
    4. Women with prothrombin G20210A mutation on estrogen replacement therapy (ERT) and with HTN have >4X increased risk for first myocardial infarction [51]
    5. Genetic risk factors have not been validated as independent for ACS [3]
  4. History of Specific Infections [56]
    1. Infection with chlamydophila, cytomegalovirus (CMV), Helicobacter pylori or herpes simplex virus (HSV) has been associated with increased risk of CVD
    2. Meta-analysis of antibiotic therapy is not associated with prevention of CAD [57]
    3. One year course of azithromycin (Zithromax®) was not effective for secondary prevention of cardiac events in patients with stable CAD [26]
    4. One year course of gatifloxacin in patients with ACS did not reduce recurrent CVD overall, even with elevated CRP [41]
    5. Presence of baseline Immunoglobulin G (IgG) to CMV, HSV, Chlamydia pneumoniae, or Helicobacter pylori did not correlate with risk of CVD in women [56]
    6. Elevated Chlamydophila pneumoniae titers did not correlate with increased risk of recurrent CVD or response to antibiotic prophylaxis [26,41]
  5. Presence of multiple complex coronary plaques on angiography associated with more severe MI and requirement for bypass surgery [58]

E. CVD Risk Reduction

  1. Risk reduction correlates with modification of biological pathways described below
  2. Green leafy vegetables and vitamin C rich fruits and vegetables reduce CAD risk [59]
  3. Exercise [96]
    1. CVD risk reduction ~30-50% for active versus sedentary lifestyle
    2. Aerobic activity may be of maximal benefit
    3. Physical activity reduces CVD mortality in smokers and nonsmokers
    4. Sudden exertion in sedentary persons is definite risk for infarction
    5. Long term excercise reduces atherogenic activity of inflammatory cells
  4. Cholesterol Reduction [61]
    1. Diet alone rarely reduces risk of ACS
    2. Statins significantly reduce total and LDL chol, CRP, primary and secondary MI risk [25,103]
    3. Statins reduce chol but also have multiple effects on other cell types
    4. Plaque stabilization and endothelial cell maintenance are enhanced by statins
    5. Reducing chol with statins in persons with high chol reduces MI risk ~30%
    6. Treatment of patients with CAD with statins reduces mortality, regardless of chol levels
    7. In patients with CAD, normal LDL (<140mg/dL) but low HDL <40mg/dL, gemfibrozil reduced initial CVD event or stroke by ~20%
    8. Low fat diets improve endothelial function in hypercholesterolemic men [62]
    9. Diets high in N-3 polyunsaturated fatty acids associated with 20-35% reduction in MI [90,93]
    10. Reduction in trans fatty acid intake is likely to reduce CAD events ~5-20% [32,46]
  5. Elevated HDL Levels
    1. HDL subtypes 2 and 3 are anti-atherosclerotic, cardioprotectants
    2. Levels of total HDL > 60mg/dL are considered protective
  6. Low Dose Aspirin (ASA) [63,64]
    1. Physicians' Health Study evaluation of low dose ASA (and many other factors) [63]
    2. Randomization to ASA or not (325mg qod) for 22,071 male physicians
    3. Total MI ~50%; 75% in fatal MI in ASA group (p<0.006 in all groups)
    4. Stroke incidence increased ~15% though p>0.1 in all (fatal, nonfatal, total) groups
    5. Accumulating data suggest that 81mg po qd is sufficient for protection [64]
    6. Risk of bleeding and possibly hemorrhagic stroke are increased with higher doses
  7. Estrogen Replacement Therapy (ERT) [65,66]
    1. Overall, ERT does not affect and might increase CVD events
    2. ERT did not affect angiographic progression of coronary artery atherosclerosis [67]
    3. Prospective study in women with history of CVD shows benefits of 0.3mg/d conjugated estrogens (equal to 0.625mg/d with fewer side effects) [68]
    4. Estrogen receptor alpha gene CC variant associated with 2X increased risk of major CAD event and 3X MI risk compared with CT or TT genotypes [108]
  8. Alcohol [70]
    1. Mild to moderate alcohol associated with >40% reduced risk of death from MI [70]
    2. Similar or greater reductions in coronary risks found in diabetics who drink [69]
    3. Alcohol associated with decrease in HDL2 and HDL3 subfractions, increased endogenous tissue plasminogen activator (TPA)
    4. No significant changes in total chol or triglycerides
    5. Mild to moderate alcohol consumption also reduces systemic inflammatory markers [71]
    6. No or marked alcohol consumption increases systemic inflammatory markers (CRP) [71]
    7. Moderate alcohol consumption in men with HTN reduces MI risk, but not mortality or overall cardiovascular risk [47]
  9. Anti-Oxidant Vitamins
    1. No clear benefit of any anti-oxidant vitamin for prevention of CAD
    2. Vitamin E 800 IU/day for 1.5 years reduced CVD 50% in dialysis patients [73]
    3. Routine vitamin supplements are not recommended for CAD or cancer prevention [105,106]
  10. Reducing Serum HC - no studies showing reduction in HC levels have definitively reduced CAD
  11. Other Factors
    1. Dietary intake of n-3 fatty acids (seafood) associated with reduced cardiac arrest
    2. High doses of folate and/or vitamin B6 (pyridoxine) may reduce serum homocysteine
    3. Ramipril, an ACE inhibitor, reduces CVD events by ~20% in patients with normal and moderate (creatinine 1.4-2.3mg/dL) renal insufficiency [4]
  12. Patients with diabetes mellitus should be aggressively treated to prevent MI
  13. Low risk CVD profile associated with ~5-10 year increased lifespan [76]
  14. Cardiac Risks in Surgery [77]
    1. Surgery is associated with increased risk of MI
    2. Patients must be evaluated pre-operatively for cardiac risks
    3. Patients at high risk for coronary events perioperatively should be carefully evaluated
    4. Bisoprolol given perioperatively to high risk patients undergoing vascular surgery reduced death and MI by >80%

F. Pathophysiology of MI [37,61]

  1. Combinations of Factors Lead to MI
    1. Presence of atherosclerosis (mainly "young" friable plaques)
    2. Predisposition to coagulopathy
    3. Platelet aggregation and thrombus formation
    4. Rupture of atherosclerotic plaque
    5. Exertion alone can lead to plaque rupture and MI or sudden death [79]
    6. Endothelial dysfunction is fundamental
    7. Atherosclerosis and thrombosis both required for most MI
  2. Prevalence of coronary occlusion during early hours of transmural MI
    1. ~90% of patients seen within 4 hours of onset of symptoms have total occlusion
    2. ~65% of patients seen 12-24 hours of onset had total occlusion
    3. ~50% of patients have a clear sympathetic (stress) related trigger event prior to MI
  3. Coronary Artery Occlusion [80,81]
    1. Arterial thrombotic occlusion is found in most cases of infarction
    2. Total occlusion usually associated with Q-wave (transmural) MI
    3. Partial (non-) occlusion usually associated with unstable angina and non-Q wave MI
    4. Coronary thrombus forms on a newly-ruptured atherosclerotic plaque
    5. Ruptured plaques expose highly thrombogenic Tissue Factor and lipid substrates
    6. Tissue Factor + Factor VIIa activates Factor X to Factor Xa
    7. Factor Xa + Factor Va cleaves prothrombin to thrombin
    8. Platelets adhere to exposed surface of ruptured plaque and activate thrombus formation
    9. Thrombus forms much as it would in a wound
    10. Most atheromata do not rupture
    11. Characteristics plaques prone to rupture have been identified (see below)
    12. Coronary artery vasospasm is responsible for occlusion in minority of cases
  4. Rupture Prone Plaques [37,61,80,81]
    1. Structural: large lipid-rich core, thin fibrous cap, reduced collagen content
    2. Exertion induced plaque rupture includes hemorrhage into plaque in >70% of cases [79]
    3. Chronic inflammation: IFNg expressing T cells, activated macrophages, mast cells
    4. Elevated levels of MIC-1 associated with increased CV risk in women [94]
    5. Increased neovascularization
    6. Reduced density of smooth muscle cells
    7. Expression of cell adhesion molecules and leukocyte activation markers
    8. Matrix metalloproteinase expression
    9. Increased tissue factor (Coagulation Factor III) expression
    10. Rupture prone plaques appear to have plaque surface irregularities [82]
    11. Persons with plaque surface irregularities have a 1.8 fold increased risk of MI than those with smooth plaques (plaques shapes assessed in the carotid arteries) [82]
  5. Involvement of Vasoconstrictors / Platelet Activators
    1. Thromboxane A2
    2. Serotonin - vasoconstrictive effects on diseased (moreso than healthy) arteries
    3. Platelet activating factor (PAF)
    4. Thrombin
    5. ADP
    6. These vasoconstrictors also stimulate platelet aggregation and thrombus formation
  6. Lack of Vasodilator Substances
    1. Insufficient nitric oxide (EDRF)
    2. Adenosine
    3. Prostacyclin
    4. Deficiencies of these substances linked to endothelial dysfunction
  7. Occlusion often resolves over next 24-48 hours without treatment
  8. Reperfusion Injury
    1. Tissue ischemia and necrosis stimulates complement and other systems
    2. Increase in neutrophil migration into dead / dying tissue
    3. Release of toxic oxygen species may contribute to injury
  9. Necrosis and Apoptosis [88]
    1. Myocyte death early in MI appears to be due to mainly to non-inflammatory apoptosis
    2. Myocyte death after >48 hours is a mixture of necrosis and apoptosis
    3. Myocyte death may always include both apoptosis and necrosis
    4. Apoptotic myocytes do not release typical cardiac enzymes such as creatine kinase
    5. Therefore, methods for detecting apoptotic myocyte cell death are needed
  10. Ischemic Myocardium Expresses Angiogenic Factors [83]
    1. Vascular endothelial growth factor (VEGF) is a key angiogenic factor
    2. Transcription factor HIF-1 (hypoxia inducible factor) stimulates VEGF mRNA expression
    3. HIF-1 mRNA is induced very early in cardiac ischemia and infarction
    4. Stimulation of angiogenesis is a goal in patients with myocardial ischemia
  11. After MI, some cardiac myocytes undergo cell division [84]

G. Prognosis

  1. Ejection Fraction (EF) is most accurate predictor of prognosis
    1. Echocardiography usually used to determine EF
    2. Radioventriculography more accurate but gives no valve function data
    3. Cardiac catheterization can provide a good estimate of EF
    4. Note that cardiac output, not just EF, is important for determining heart function
  2. Complications post-MI indicate poor prognosis
    1. Arrhythmias
    2. Bundle branch block
    3. Congestive Heart Failure
  3. Even asymptomatic ventricular arrhythmias have 2 fold increased incidence of death
  4. Stress thalium test may be done 3-6 weeks post-MI
    1. Exercise test preferred to evaluate functional status
    2. Thalium should be used to assess dead versus ischemic myocardium
    3. Determine if coronary angiography is indicated
    4. That is, is there additional myocardium at risk?
  5. Overall, women have more lethal and severe first MI than men
    1. Increased risk of acute pulmonary edema or cardiogenic shock
    2. Increased 28 day mortality (18% for women versus 8% for men)
    3. Increased 6-month mortality rates (23% for women versus 12% for men)
  6. Renal insufficiency is an independent risk for death in elderly patients with MI [98,99]

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