Ischemic Heart Disease and Angina Pectoris

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Questions and Answers

In the context of ischemic heart disease, which statement BEST encapsulates the role of endothelial dysfunction?

  • It primarily affects the oxygen-carrying capacity of hemoglobin, leading to reduced myocardial oxygen supply.
  • It solely impacts the contractility of the myocardium, increasing oxygen demand without affecting coronary blood flow.
  • It impairs the release of vasodilators and antithrombotic factors, exacerbating vasoconstriction and promoting thrombosis. (correct)
  • It directly causes fixed vessel narrowing due to the proliferation of smooth muscle cells within the arterial lumen.

Considering the interplay of factors influencing coronary vascular tone, what is the MOST nuanced understanding of catecholamine stimulation's effect on coronary arteries?

  • Catecholamine stimulation invariably leads to coronary vasoconstriction via α-adrenergic receptor activation, irrespective of metabolic demands.
  • Initial vasoconstriction via α-adrenergic receptors may be superseded by vasodilation mediated by local metabolites responding to increased myocardial oxygen consumption. (correct)
  • Catecholamine stimulation predominantly causes coronary vasodilation through β2-adrenergic receptors, ensuring adequate myocardial perfusion.
  • Catecholamine stimulation has no direct impact on coronary vascular tone; its effects are solely determined by local metabolic factors.

Which of the following statements BEST synthesizes the role of ventricular hypertrophy in the context of myocardial oxygen balance?

  • Ventricular hypertrophy has no significant impact on myocardial oxygen balance; it only affects the electrical properties of the heart.
  • Ventricular hypertrophy invariably increases myocardial oxygen consumption due to the increased muscle mass.
  • Ventricular hypertrophy serves solely as a maladaptive response that exacerbates ischemia by increasing wall stress.
  • Ventricular hypertrophy initially compensates by reducing wall stress, but may become insufficient as oxygen demand outpaces supply. (correct)

In the continuum of ischemic syndromes, what is the defining characteristic that differentiates unstable angina from stable angina?

<p>A pattern of increasing frequency and duration of ischemic episodes, occurring with less exertion or at rest. (C)</p> Signup and view all the answers

Which pathophysiological mechanism BEST describes the phenomenon of 'stunned myocardium'?

<p>Prolonged systolic dysfunction following an episode of acute, transient ischemia despite restored blood flow. (D)</p> Signup and view all the answers

Considering Poiseuille's Law, which BEST explains the hemodynamic impact of a stenotic lesion on coronary artery blood flow?

<p>Blood flow is inversely proportional to the vessel radius raised to the fourth power, highlighting the exponential impact of vessel narrowing. (C)</p> Signup and view all the answers

Which of the following BEST describes the rationale behind using a combination of aspirin and a P2Y12 ADP receptor antagonist in managing ischemic heart disease?

<p>To provide synergistic antiplatelet effects by targeting different pathways of platelet activation and aggregation. (D)</p> Signup and view all the answers

What is the MOST critical consideration when interpreting the results of coronary angiography in the context of potential revascularization?

<p>Both the anatomical severity of stenoses and their functional consequences through symptoms and myocardial viability. (B)</p> Signup and view all the answers

In the management of acute stable angina, what is the MOST precise pharmacological mechanism by which sublingual nitroglycerin alleviates symptoms?

<p>Primarily causing systemic venodilation, thereby reducing preload and myocardial oxygen demand. (C)</p> Signup and view all the answers

Regarding the long-term management of chronic stable angina, what is the MOST accurate understanding of the role and limitations of organic nitrates?

<p>They are used purely for symptomatic relief by causing vasodilation but do not improve survival or prevent myocardial infarctions. (C)</p> Signup and view all the answers

Considering the contraindications and potential adverse effects, which represents the MOST judicious approach to prescribing beta-blockers for chronic stable angina?

<p>Use beta-1 selective blockers with caution in those with asthma or significant obstructive airway disease. (B)</p> Signup and view all the answers

How does ranolazine, as an anti-ischemic agent, differ mechanistically from traditional therapies such as beta-blockers and nitrates?

<p>It decreases the frequency of anginal episodes and improves exercise capacity without affecting heart rate or blood pressure. (C)</p> Signup and view all the answers

In the management of chronic stable angina, what is the MOST compelling rationale for the use of HMG-CoA reductase inhibitors (statins)?

<p>To lower LDL cholesterol and reduce cardiovascular clinical events (MI and death), mediated by plaque stabilization and improved endothelial function. (C)</p> Signup and view all the answers

In patients with chronic stable CAD, beyond antianginal medications, which adjunctive pharmacological intervention BEST addresses long-term cardiovascular risk reduction?

<p>High-intensity statin therapy to achieve aggressive LDL cholesterol reduction alongside antiplatelet therapy. (C)</p> Signup and view all the answers

Considering the decision between PCI and CABG for revascularization, which patient profile would MOST strongly favor CABG?

<p>A patient with severe LV systolic dysfunction and multivessel disease, including a critical narrowing of the proximal left anterior descending artery. (B)</p> Signup and view all the answers

Following coronary artery stent placement, which medication regimen is MOST crucial to prevent stent thrombosis and maintain arterial patency?

<p>Combination of aspirin plus a P2Y12 receptor antagonist for at least 12 months, followed by aspirin indefinitely. (D)</p> Signup and view all the answers

What is the MOST accurate assessment of the role of percutaneous coronary intervention (PCI) in the context of stable coronary artery disease?

<p>PCI has not been shown to reduce the risk of MI or death. (B)</p> Signup and view all the answers

In the contemporary management of chronic ischemic heart disease, which of the following therapeutic strategies BEST targets the thrombotic component of acute coronary syndromes?

<p>Employing antiplatelet agents, such as aspirin and P2Y12 receptor antagonists, to inhibit platelet activation and aggregation. (D)</p> Signup and view all the answers

Considering the role of sodium handling in blood pressure regulation, which mechanism BEST explains how kidney dysfunction leads to hypertension?

<p>Damaged nephrons are unable to excrete normal amounts of sodium and water. (C)</p> Signup and view all the answers

Secondary hypertension can manifest the following clinical clues, which could have a similar presentation with congestive heart failure?

<p>Pulmonary edema with a normal serum chemistry test. (B)</p> Signup and view all the answers

The role as renal component of BP, could be explained by this statement:

<p>No matter how high the CO or TPR, renal excretion has the capacity to completely return BP to normal by reducing intravascular volume. (A)</p> Signup and view all the answers

Transplantation effects on patients are a good marker, and a study has confirmed that:

<p>Patients who donate kidneys to hypertensive rats will likely increase high blood pressure rate by hereditary functions. (A)</p> Signup and view all the answers

Why is it important to test hormone levels when trying to find a direct relation between blood pressure and an endocrine cause?

<p>Circulating hormones play an important role, so it should not be surprising that endocrine diseases cause hypertension. (D)</p> Signup and view all the answers

The natural state of hypertension is due to what?

<p>BP is elevated over long durations. (A)</p> Signup and view all the answers

Flashcards

Ischemic heart disease

Imbalance between myocardial oxygen supply and demand.

Angina pectoris

Uncomfortable sensation in the chest and neighboring structures due to myocardial ischemia.

Stable angina

Transient angina pectoris precipitated by physical activity or emotional upset, relieved by rest.

Variant angina

Anginal discomfort, usually at rest, due to coronary artery spasm.

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Silent ischemia

Asymptomatic episodes of myocardial ischemia.

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Unstable angina

Increased frequency and duration of angina episodes produced by less exertion or at rest.

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Ventricular wall stress

Tangential force acting on myocardial fibers.

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Fixed Vessel Narrowing

Fixed atherosclerotic plaques narrow vessel lumen, limiting blood supply.

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Magnitude of proximal arterial stenosis

Resting and maximal coronary blood flows are affected by the magnitude of proximal arterial stenosis.

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Endothelial Cell Dysfunction

Abnormal endothelial cell function contributes to the pathophysiology of ischemia by vasoconstriction of coronary arteries.

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Consequences of Ischemia

The reduced generation of ATP impairs the interaction of the contractile proteins.

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Stunned myocardium

Prolonged systolic dysfunction after severe acute, transient ischemia exhibits returns to normal systolic function.

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Hibernating myocardium

The tissue that manifests chronic ventricular contractile dysfunction due to a persistently reduced blood supply.

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Stable Angina's Cause

Inadequate oxygen supply for high myocardial oxygen demands.

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Vasoconstriction contributing to ischemia

Endothelial Dysfunction, leading to paradoxical vasoconstriction.

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Unstable Angina

Sudden increase in tempo and duration of ischemic episodes.

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Variant Angina

Focal coronary artery spasm results in intense vasospasm alone reduces coronary oxygen supply .

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Silent Ischemia

Cardiac ischemia that occurs in the absense of symptoms.

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Clinical Evaluation of Ischemic Heart Disease.

The single most important component is the history described by the patient.

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Physical Examination

Physical exam assesses for signs of atherosclerotic disease.

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Electrocardiogram (ECG)

Detects heart rate and rhythm/ST-segment and T-wave changes during ischemia.

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Standard Exercise Testing

Observes chest discomfort, ECG abnormalities and how long a patient can exercise.

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Radionuclide Imaging Studies

Reveals impaired perfusion.

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Exercise Echocardiography

Uses echocardiography to assesses for regional ventricular dysfunction.

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Pharmacologic Stress tests

Vasodilates, but often used when patients cant exercise; can also use dobutamine.

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Coronary Angiography

Identifies the degree of stenosis

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Coronary Angiography limitations

Provides only anatomic information

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Coronary CT Angiography (CCTA)

visualize the coronary arteries.

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The complete lack of CAC

Indicates the absence of CAD

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Treatments

Decrease the frequency and prevent acute episodes/ events, prolong survival.

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Sublingual nitroglycerin

The drug of choice in the setting of acute angina.

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Beta Blockers Role

Relieving ischemia by reducing myocardial oxygen demand.

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Beta blockers

First-line chronic therapy for ischemic heart disease.

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Organic nitrates

Relieve ischemia primarily through vascular smooth muscle relaxation.

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Nondihydropyridine calcium channel blockers

Antianginal effects stemming from potent cardiac depressant actions

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Ranolazine

Shown to decrease rate of anginal episodes and improve exercise capacity.

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Aspirin role

antiplatelet therapy reduces the risk of acute events.

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Lipid lowering therapy

Lower MI and death rates especially in patients with CAD.

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Revascularization Pursued

Surgical, is pursued if patients angina does not respond adequately to drug therapy

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Coronary Stents

Coronary stents significantly reduce the rate of stenosis.

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Study Notes

  • In ischemic heart disease, angina pectoris is the most common syndrome, defined as an uncomfortable sensation in the chest due to an imbalance between myocardial oxygen supply and demand.
  • Ischemic heart disease results from an imbalance between myocardial oxygen supply and demand leading to myocardial hypoxia and accumulation of waste metabolites, frequently due to coronary artery atherosclerosis.
  • Angina pectoris is discomfort in the chest resulting from myocardial ischemia.
  • Stable angina is a pattern of transient angina triggered by physical activity or emotional stress, relieved by rest, and often linked to temporary ST segment depression.
  • Variant angina presents typical anginal discomfort, mainly at rest, due to coronary artery vasospasm, often ST segment elevation, and is also called Prinzmetal angina.
  • Silent ischemia involves asymptomatic episodes of myocardial ischemia, identified via electrocardiogram and other lab tests.
  • Unstable angina includes increased frequency and longer angina episodes triggered by less exertion or at rest, at high risk of developing myocardial infarction if not treated.
  • Major determinants of oxygen supply include O2 content and coronary blood flow.
  • Coronary blood flow depends on coronary artery perfusion directly and inversely on coronary vascular resistance
  • Coronary perfusion mainly takes place during diastole rather than systole due to myocardium contraction during systole.
  • Lower aortic diastolic pressure reduces myocardial oxygen supply.
  • Coronary vascular resistance is modified by external compression and intrinsic coronary tone.
  • The subendocardium is more vulnerable to ischemic damage because of greater force during myocardial contraction.
  • The heart increases blood flow to meet oxygen demands because it cannot increase oxygen extraction.
  • Autoregulation of coronary vascular resistance is the most important mediator of arterial tone.
  • The discovery of nitric oxide helped explain this effect.
  • Local metabolites affect coronary vascular tone, modulating oxygen supply to meet changing metabolic demands; adenosine is a potent vasodilator.
  • Endothelial cells produce vasoactive substances which contribute to regulation of arterial tone that includes nitric oxide (NO), prostacyclin, and endothelium-derived hyperpolarizing factor (EDHF).
  • In the normal state, vasodilation from substances like nitric oxide and prostacyclin predominates.
  • The neural control of vascular resistance has empathetic and parasympathetic control, and catecholamine stimulation may cause vasoconstriction or vasodilation .
  • Major determinants of myocardial oxygen demand are ventricular wall stress, heart rate, and contractility.
  • Wall stress related to intraventricular pressure, radius of the ventricle, and wall thickness can be estimated using Laplace's relationship.
  • Conditions that augment left ventricular filling raise wall stress and oxygen consupmtion.
  • Hypertrophy serves as a compensatory role reducing oxygen consumption.
  • Myocardial contractility augments the force of contraction, which increases oxygen consumption.
  • Myocardial ischemia in CAD is from fixed atherosclerotic plaques.
  • Vascular resistance is governed by vessel length and its radius.
  • Hemodynamic significance of a coronary artery stenosis depends on both the degree of epicardial portion vessel narrowing and the amount of compensatory vasodilatation distal resistance vessels can do.
  • If a stenosis narrows the lumen diameter by <60%, the arteries do not get significantly altered
  • A stenosis that reduces the coronary blood flow increases myocardial ischemia.
  • Another contributor to reduced myocardial oxygen supply is endothelial dysfunction by inappropriate vasoconstriction and loss of normal antithrombotic properties.
  • Physical activity or mental stress results in measurable coronary artery vasodilatation with activation of the sympathetic nervous system.
  • The resultant decrease in coronary blood flow contributes to ischemia from direct catecholamine effect.
  • Factors released from endothelial cells also exert antithrombotic properties which are lowered with dysfunction.
  • Factors can result in an imbalance between myocardial oxygen supply and demand.
  • The inadequate myocardial oxygenation and local accumulation of waste products characterize the consequences of ischemia.
  • Myocytes convert from aerobic to anaerobic metabolic pathways resulting in reduced ATP impairs and results in a transient reduction of both ventricular systolic contraction and diastolic relaxation.
  • Ischemic insults can result in a period of prolonged contractile dysfunction without necrosis and recovery.
  • Stunned myocardium tissue demonstrates prolonged systolic dysfunction after severe acute transient ischemia and contractile function gradually recovers.
  • Clinical syndromes that result depend on the underlying pathophysiologic process and timing of myocardial ischemic insult.
  • Chronic stable angina manifests as a pattern of predictable, transient chest discomfort during exertion or emotional stress, due to fixed obstructive atheromatous plaque.
  • Inadequate oxygen supply in stable angina is inappropriate vasoconstriction by associated atherosclerosis endothelial dysfunction, leading vessels to paradoxically vasoconstrict.
  • A patient with chronic stable angina may experience a sudden increase in the tempo and duration of ischemic episodes, know as unstable angina, which can be a precursor to an acute MI.
  • A small minority exhibit focal coronary artery spasm in absence of lesions.
  • Episodes of cardiac ischemia that happen in the absence of perceptible discomfort or pain are silent ischemia.
  • Episodes are more common among patients with diabetes, elderly, and women.
  • Microvascular angina refers to angina pectoris in the absence coronary stenoses on coronary angiography but it was not well understood.
  • To evaluate for chronic stable angina a medical professional interviews and examines a patient during an actual angina episode.
  • Patients with chronic stable angina describe a pressure, discomfort, tightness, burning in the chest.
  • Acute anginal attacks also produces generalized sympathetic and parasympathetic stimulation resulting in tachycardia, diaphoresis, and nausea.
  • Angina is precipitated by conditions that increase myocardial oxygen demand (eg, increased heart rate, contractility, or wall stress).
  • History of pre-existing conditions with atherosclerosis and CAD include risk factors cigarette smoking, dyslipidemia, hypertension, diabetes, and a family history of premature coronary.
  • Differentiate from other cardiac causes (eg, pericarditis), gastrointestinal disorders (eg, gastroesophageal reflux, peptic ulcer disease, esophageal spasm, or biliary pain), and musculoskeletal conditions (including chest wall pain, spinal osteoarthritis, and cervical radiculitis).
  • If possible to examine a patient during an attacks, transient physical signs could be detected like increased heart rate and blood pressure are common due to the sympathetic response
  • Also assess for signs of atheroselerotic disease through other vascular beds.
  • Diagnostic studies can comfirm myocardial ischemia as an ECG.
  • During myocardial ischemia, ST-segment and T-wave changes can appear.
  • Stress testing involves provocative exercise or pharmacologic stress to assess for heart disease.
  • A standard exercise test is performed in those suspected of having CAD.
  • Since a standard exericse testing relies on ECG it is less for in patients with abormalities.
  • Radionuclide imaging is combined with exercise testing.
  • Pharmocologic stress testing is available for individuals unable to do the exercise.
  • Use vasodilator such as adenosine adenosine to test.
  • Gold testing for artrey stensoses is coronary angiography.
  • Non invasive imagine of artery exists through noninvasively viewing of the artery.
  • In summary, goal is to:
  • reduce the frequency of anginal attacks,
  • to prevent acute coronary syndromes such as MI, and
  • to prolong survival.
  • The first line of defence is pharmocologic agents that decreased cardiac workload and more perfusion. Therre are three types of medication that are commonly used organic nitrates, ß-adrenergic blockers, and calcium channel blockers
  • The organic nitrates are used to treat severe attacks, they are an organic nitrite, which is the drug of choice,
  • The drug is placed under tongue and begins to take effect in 1-2 minutes.
  • -Blockers (see Chapter 17) exert their antianginal effect primarily by reducing myocardial oxygen demand, and suppressing angina.
  • Pharmacologic agents are used to prevent acute coronary syndromes with aspirin and platelet P2Y12 ADP receptor antagonists.
  • Lipis lowering treatment should be employed using HMG-CoA reductase inhibitors to to reduce cardiovasuclar clinical events.
  • In cases of having chronic CAD with a glucose lowering they use sodium-glucose cotransporter 2 [SGLT2] inhibitors and glucagon-like peptide-1 [GLP-1] receptor agonists to decrease event rates.
  • Revasculiztion is a Coronary Artery Bypass Graft Surger (CABG) or Percutaneous Coronary Interventions (PCI) and is pursued when medical therapy is not working,.

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