Flashcards in Goldman Deck (40)
What is ischemic heart disease caused by?
obstruction or stenosis of one or more of the epicardial coronary arteries by atheromatous plaque
What is angina pectoris caused by?
generally a consequence of a supply-demand imbalance: an activity increases cardiac workload or “demand,” thereby resulting in an increase in heart rate, blood pressure, and contractility, leading to an increase in left ventricular (LV) wall tension; but stenotic coronary arteries are unable to augment antegrade flow or “supply” adequately in response to this increase in demand.
Such an imbalance classically results in chest discomfort
What is angina pectoris?
discomfort in the chest or adjacent areas caused by myocardial ischemia.
How is angina pectoris graded?
The Canadian Cardiovascular Society (CCS) angina grading scale is a widely used four-point ordinal scale that classifies angina pectoris from mild (class I: angina occurring only during strenuous or prolonged physical activity) to severe (class IV: inability to perform any activity without angina, or angina at rest) and includes the full spectrum of angina from chronic stable to unstable
For classification purposes, subjects with stable ischemic heart disease generally exhibit CCS class I-II symptoms, which are typically provoked by exertion.
Other grading systems include a specific activity scale, which is based on the metabolic cost of specific activities, and an anginal score, which integrates the clinical features and tempo of angina with electrocardiographic changes and offers independent prognostic information beyond that provided by age, gender, ventricular function, and coronary anatomy.
Incidence of angina pectoris?
Among individuals aged 45 years and older, the incidence of stable angina pectoris is about 500K per year, of whom about 65% are men
When does ischemia arise?
which rapidly develops when a mismatch arises between myocardial oxygen needs and myocardial oxygen supply
How does ischemia manifest clinically?
variable ranging from no symptoms (e.g., silent myocardial ischemia) to angina as a precursor to unstable angina, myocardial infarction (MI), or sudden cardiac death
Two major pathogenetic mechanisms may result in myocardial ischemia and angina in the chronic setting
so-called demand angina, which is caused by an increase in myocardial oxygen requirements and workload; and supply angina, which is caused by diminished oxygen delivery to myocardial tissue.
Demand angina is a consequence of the increased myocardial oxygen requirements that occur with what things commonly?
increased physical activity, emotion, or stress.
In a patient with chronic, restricted oxygen delivery due to atherosclerotic narrowing of a coronary artery, this increased demand may precipitate angina.
Other extracardiac precipitants of angina include the excessive metabolic demands imposed by
-severe anemia from blood loss,
-tachycardia from any cause
The pathophysiologic basis for angina and ischemia in patients with stable ischemic heart disease has important implications for the selection of anti-ischemic agents.
The greater the contribution from increased myocardial oxygen requirements to the imbalance between supply and demand, the greater the likelihood that agents that reduce heart rate and wall tension, such as β-blockers or non-dihydropyridine calcium antagonists, will provide clinical benefit, whereas nitrates and calcium antagonists with more potent vasodilatory properties (particularly the dihydropyridines) will be more beneficial to alleviate angina and ischemia mediated by coronary vasoconstriction.
What is the most common cause of ischemic heart disease?
atherosclerotic narrowing of the coronary arteries resulting in flow-limiting obstruction to epicardial blood flow
What are some nonatherosclerotic causes of obstructive coronary artery disease?
-congenital abnormalities of the coronary arteries,
-coronary arteritis in association with systemic vasculitides, and
-radiation-induced coronary disease.
How can radiation cause obstructive disease?
Radiation therapy for thoracic or mediastinal malignant neoplasms, particularly breast cancer and Hodgkin lymphoma, can cause long-term coronary microangiopathy and macroangiopathy.
There is a four- to seven-fold increase in clinically significant, high-grade coronary artery stenosis of the mid and distal left anterior descending coronary artery in women with irradiated left-sided breast cancer compared with those treated with radiation for right-sided breast cancer.
How else might myocardial ischemia and angina pectoris occur?
in the absence of obstructive coronary artery disease, as in the case of aortic valve disease, hypertrophic cardiomyopathy, and dilated cardiomyopathy.
What is acute coronary syndrome?
used to describe the continuum of myocardial ischemia (unstable angina pectoris) or infarction (with or without concomitant ST segment elevation)
What is unstable angina?
The patient with unstable angina has cardiac chest pain that is new, worsening (i.e., more severe, prolonged, or frequent than previous episodes of angina), or occurring at rest, without serologic evidence of myocyte necrosis—that is, no elevation of serum concentrations of troponin or the MB isoenzyme of creatine kinase (CK-MB) and no ST elevation
What is a non-ST segment elevation MI ?
The patient with cardiac chest pain WITH serologic evidence of myonecrosis but without ST segment elevation
T or F. Both unstable angina and non-ST segment elevation MI are termed non-ST segment elevation ACS
T. aka NSTE ACS. Because unstable angina and non–ST segment elevation MI are characterized by the absence of ST segment elevation
What is an ST segment elevation MI (STEMI)?
If the involved coronary artery is *totally occluded* by fresh thrombus, the patient with acute-onset cardiac chest pain, serologic evidence of myonecrosis, and persistent (>20 minutes) ST segment elevation as revealed from an ECG is said to have an ST segment elevation MI
What is a primary ACS?
is precipitated by rupture of a coronary arterial atherosclerotic plaque, with subsequent platelet aggregation and thrombus formation, leading in turn to diminished blood flow in the involved artery
What is a secondary ACS?
caused by a transient or sustained marked imbalance between myocardial oxygen supply and demand
Causes of secondary ACS?
Substantial reductions in oxygen supply, for example, can be caused by severe systemic arterial hypotension, anemia, or hypoxemia; dramatic increases in oxygen demand can be caused by tachycardia, severe systemic arterial hypertension, or thyrotoxicosis.
treat the underlying cause
What is the precipitating event in almost all subjects with NSTE ACS?
coronary arterial atherosclerotic plaque rupture or erosion, with subsequent platelet aggregation and thrombus formation, leading to subtotal occlusion of the involved artery.
In an occasional patient, total thrombotic occlusion of the artery leads to NSTE ACS rather than to ST segment elevation MI when extensive collateral blood supply perfuses the region of myocardium that is distal to the occluded artery.
Other causes of NSTE ACS?
- Rarely, intense vasospasm of a segment of an epicardial coronary artery, due to focal endothelial dysfunction (i.e., Prinzmetal's angina)
- drug ingestion (caused, for example, by cocaine, chemotherapeutic agents, or one of the serotonin receptor agonist “triptans”), causes a transient or sustained compromise of coronary arterial blood flow, with resultant NSTE ACS.
- Spontaneous coronary arterial dissection, which occurs most often in peripartum women and patients with vasculitis, may result in NSTE ACS.
What factors help erode the fibrous cap of a coronary arterial atherosclerotic plaque to precipitate NSTE ACS?
Local and systemic inflammation, mechanical features, and anatomic changes contribute to the transformation of a stable atherosclerotic plaque to a so-called vulnerable plaque, the rupture of which triggers platelet adherence, activation, and aggregation, with subsequent thrombus formation.
What stimulates this inflammatory response?
The deposition of oxidized LDL in the coronary arterial wall stimulates an inflammatory response, which results in the accumulation of macrophages and T lymphocytes at the plaque border.
What do the inflammatory cells do?
These inflammatory cells secrete cytokines (e.g., tissue necrosis factor, interleukin-1, interferon-γ), which inhibit collagen synthesis and deposition, as well as enzymes (e.g., matrix metalloproteinases and cathepsins), which promote collagen and elastin degradation, thereby rendering the overlying fibrous cap vulnerable to rupture.