Figure 88.1. The Framingham 10-year Cardiovascular Disease Risk Calculator. Point of care assessment for cardiovascular disease risk may be performed using various validated risk models. In the Framingham risk calculator, the 10-year probability of developing a myocardial infarction is based on age, cholesterol levels, systolic blood pressure, cigarette smoking history, and diabetes mellitus status.
Source: Adapted with permission from Wilson PW, D’Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB. Prediction of coronary heart disease using risk factor categories. Circulation. 1998;97:1837–1847.
Table 88.1 TREATMENT GOALS FOR PLASMA LOW DENSITY LIPOPROTEIN (LDL) LEVELS ACCORDING TO 10-YEAR CARDIOVASCULAR RISK
NOTES: The preferred treatment strategy for hypercholesterolemia depends, in part, upon the relationship between plasma LDL levels and the number of cardiovascular risk factors for an individual patient. (A) The timing for initiating therapeutic change to lifestyle (i.e., goal-directed diet and exercise; refer to Figure 87.3 for more detail on behavioral modification recommendations) and drug therapy is outlined for patients with ≥2 cardiovascular risk factors. Note that in patients with very high risk, defined as CVD and one or more of: diabetes mellitus, multiple major risk factors, poorly controlled risk factors, metabolic syndrome, or acute coronary syndrome, an optional target LDL <70 mg/dL is preferred if this can be achieved safely. (B) Recommendations for patients with ≤1 risk factor. Pharmacotherapy after lifestyle modification is reasonable in patients with 0-1 risk factor and LDL level 160–190 mg/dL.
SOURCE: Reproduced with permission from National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Circulation 2007;106:3143–3421.
Figure 88.2. A model of steps in therapeutic lifestyle changes (TLC).
Source: Reproduced with permission from National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Circulation 2007;106:3143–3421.
Table 88.2 GUIDE TO CVD RISK REDUCTION
| RISK FACTOR | APPARENTLY HEALTHY PATIENTS | SECONDARY PREVENTION |
Smoking cessation | Complete cessation | Complete cessation |
Hypertension | <140/90 mm Hg | <130/80 mm Hg for patients with diabetes or chronic kidney disease |
High cholesterol | LDL-C <160 mg/dL if patient has 0–1 other risk factors, * <130 mg/dL if two or more risk factors; also HDL-C >40 mg/dL and TG <200 mg/dL | Primary goal: LDL-C ≤100 and preferably ≤70 mg/dL. Secondary goal: HDL-C >40 mg/dL and TG <200 mg/dL |
Physical inactivity | 30 min of moderate physical activity on most, if not all, days of the week. | 30 min of moderate physical activity on most, if not all, days of the week |
Weight | BMI <25 kg/m2, waist circumference <40 inches for men and <35 inches for women; at a minimum, no increase in weight | BMI <25 kg/m2, waist circumference <40 inches for men and <35 inches for women; at a minimum, no in crease in weight |
Glucose control | Goal: HbA1c <7%. First-step therapy: weight reduction and exercise Second-step therapy: oral hypoglycemic agents Third-step therapy: insulin | |
Menopause | Combined estrogen plus progestin should not be used to prevent CVD in postmenopausal women | Combined estrogen plus progestin should not be used to prevent CVD in postmenopausal women |
Antioxidants | Antioxidant supplements should not be used to prevent CVD | Antioxidant supplements should not be used to prevent CVD |
Psychosocial | Evaluate for depression/anxiety disorders. Assess structural/functional support. | Evaluate for depression/anxiety disorders. Assess structural/functional support. |
Antiplatelet agents | Aspirin, 75–162 mg/day; Clopidogrel, 75 mg/day for at least 1 month after BMS and at least 1 year after DES; long-term therapy (e.g., 1 year) after UA/NSTEMI and STEMI. | |
RAAS inhibition | ACE inhibitors or ARBs for patients with LVEF ≤40% and those with hypertension, diabetes, chronic kid- ney disease | |
Beta blockers | For all patients who have had an ACS or LV dysfunction with or without HF symptoms | |
Influenza vaccination | All patients with CVD should have an annual influenza vaccination | |
NSAIDs | Avoid if possible but use stepped care approach† if required to control musculoskeletal symptoms |
NOTES: * Risk factors include age (men ≥45 years, women ≥55 years or postmenopausal), smoking, hypertension, diabetes, family history of congestive heart disease in first-degree relative, and HDL-C <40 mg/dL. If HDL-C ≥60 mg/dL, subtract one risk factor. BMI, body mass index; BP, blood pressure; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; TG, triglycerides; RAAS, renin-angiotensin-aldosterone-sympathetic axis; NSAIDs, non-steroidal anti-inflammatory. LVEF, left ventricular ejection fraction; BMS, bare metal stent; DES, drug eluting stent; HF, heart failure.
SOURCES: Modified from: (1) Meadows J, Danik JS, Albert MAA. Primary prevention of ischemic heart disease. In: Antman EM (ed.), Cardiovascular Therapeutics: A Companion to Braunwald’s Heart Disease, 3rd ed. (pp. 208–9). Philadelphia: WB Saunders/Elsevier, 2007; (2) Antman EM, Hand M, Armstrong PW, et al. 2007 focused update of the ACC/AHA 2004 Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction. Circulation. 2008;117:296–329; (3) Anderson JL, et al. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non ST-Elevation Myocardial Infarction). Circulation. 2007;116:e148–304.
ATHEROSCLEROTIC VASCULAR DISEASE
Atherosclerosis describes a process in which various maladaptive cellular and molecular events within the blood vessel wall promote an arteriopathy that is characterized by luminal occlusion, abnormal vascular reactivity, and a predilection for thrombosis (i.e., atherosclerotic plaque rupture). Atherosclerosis may affect any vascular bed, although the most common (and often most critical) clinical presentation of atherosclerotic disease involves the coronary, cerebrovascular, and peripheral arterial circulation in which impaired blood flow is expressed as myocardial ischemia (angina pectoris/acute coronary syndrome), stroke, and claudication/critical limb ischemia, respectively.
Generally, atherosclerotic disease causes symptoms when blood vessel narrowing limits perfusion to a target organ. In the case of IHD, changes to myocardial oxygen demand due to increased heart rate, myocardial contractility, or myocardial wall stress that are not met with a proportional increase in coronary artery perfusion because of atherosclerosis-mediated narrowing of epicardial coronary arteries results in myocardial ischemia. This may present clinically as exertional angina pectoris or an angina equivalent such as dyspnea at varying degrees of exercise intensity (table 88.3). Cardiac angina due to a myocardial supply–demand mismatch is a distinct pathophysiological process from acute myocardial infarction, in which sudden rupture of an atherosclerotic plaque triggers thrombosis and, subsequently, total or subtotal occlusion of coronary blood flow and myocardial injury or necrosis (see Acute Myocardial Infarction section below).
Table 88.3 THE CANADIAN CARDIOVASCULAR SOCIETY ANGINA SCORE
SOURCE: Adapted from L Campeau. The Canadian Cardiovascular Society grading of angina pectoris revisited 30 years later. J Can Cardiovasc Soc. 2002;18:371–379.
Once the diagnosis of IHD is established through history, physical examination, stress testing, nuclear perfusion imaging, and/or cardiac angiography, the clinical management involves a combination of pharmacotherapeutic interventions to decrease demand ischemia and minimize risk factors for developing an acute myocardial infarction. In patients for whom symptoms of cardiac angina persist despite optimal medical therapy or progress to include high-risk features such as rest or crescendo angina, percutaneous coronary intervention with balloon angioplasty/coronary stent placement or coronary artery bypass surgery may be indicated. A guide to the selection of exercise stress test, nuclear perfusion imaging, and/or coronary angiography for the diagnosis of IHD is provided in Figure 88.3.
Figure 88.3. Flow chart demonstrating the recommendations of appropriateness for exercise stress test, nuclear perfusion imaging, and invasive angiography for the diagnosis or risk stratification of ischemic heart disease.
Source: Reproduced with permission from Gibbons RJ, et al. ACC/AHA/ACP-ASIM guidelines for the management of patients with chronic stable angina: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Chronic Stable Angina). J Am Coll Cardiol 33:2092–2197, 1999 and Maron BA and O’Gara PT. The evaluation and clinical management of chronic ischemic heart disease. In Hurst’s: The Heart (Fuster, Walsh, Harrington) 13th ed. McGraw/Hill Press. June 2011.
ACUTE CORONARY SYNDROME
Disruption of a lipid-laden plaque in an epicardial coronary artery exposes tissue factor and oxidized low density lipoprotein (LDL) to the passing bloodstream, setting in motion platelet adhesion, activation, and aggregation as well as initiation of the coagulation cascade. Under these circumstances, the patient may present with a range of symptoms including ischemic chest discomfort; nausea; dizziness, arm, abdominal, or jaw pain; syncope; and other angina-equivalent symptoms. The 12-lead electrocardiogram (ECG) and assessment of cardiac enzymes (i.e., cardiomyocyte injury-specific troponin I and T) from the peripheral blood assist in establishing a diagnosis of acute coronary syndrome (ACS). The term ACS refers to a spectrum of conditions including unstable angina (UA), non–ST elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI) (Figure 88.4). In UA, history and physical examination findings suggest intermittently impaired coronary blood flow due to an unstable but as yet unruptured atherosclerotic plaque. Electrocardiographic findings of cardio myocardial ischemia, such as ST-segment depression, may also be observed in UA. By contrast, biomarkers of cardio myocyte necrosis, which is indicative of myocardial infarction, is not part of UA. Thus overall, UA is a clinical diagnosis. This differs from NSTEMI and STEMI, which are defined as forms of myocardial infarction that may be subendocardial or transmural.
Figure 88.4. Acute Coronary Syndromes. After disruption of a vulnerable or high-risk plaque, patients experience ischemic discomfort that results from a reduction of flow through the affected epicardial coronary artery. The flow reduction may be caused by a completely occlusive thrombus (right side) or subtotally occlusive thrombus (left side). Patients with ischemic discomfort may present with or without ST-segment elevation on the ECG. Among patients with ST-segment elevation, most (thick white arrow in bottom panel) ultimately develop a transmural, myocardial infarction (QwMI), although a few (thin white arrow) develop a non–Q-wave (non-transmural) MI (NQMI). Patients who present without ST-segment elevation are suffering from either unstable angina (UA) or a non–ST-segment elevation MI (NSTEMI) (thick red arrows), a distinction that is ultimately made on the basis of the presence or absence of a serum cardiac marker such as CK-MB or a cardiac troponin detected in the blood. Most patients presenting with NSTEMI ultimately develop a NQMI on the ECG; a few may develop a QwMI. The spectrum of clinical presentations ranging from UA through NSTEMI and STEMI is referred to as the acute coronary syndromes.
Source: Figure and legend adapted from Anderson JL, et al.: American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2011 ACCF/AHA focused update incorporated into the ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the American Academy of Family Physicians, Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2011;10(19):e215–367.
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