How is coronary blood flow improved in the treatment of myocardial ischemia?
By reversing vasoconstriction, preventing clotting, and reducing plaque growth and rupture.
Why is it important to recognize unstable angina?
It signals that the atherosclerotic plaque has ruptured, and infarction may soon follow.
1/190
p.3
Evaluation and Treatment of Myocardial Ischemia

How is coronary blood flow improved in the treatment of myocardial ischemia?

By reversing vasoconstriction, preventing clotting, and reducing plaque growth and rupture.

p.5
Acute Coronary Syndromes and Myocardial Infarction

Why is it important to recognize unstable angina?

It signals that the atherosclerotic plaque has ruptured, and infarction may soon follow.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What diagnostic tests are used to identify unstable plaques before they rupture?

Intravascular ultrasound or MRI, angioscopy, and spectroscopy.

p.5
Evaluation and Treatment of Myocardial Ischemia

What other medications may be used in the management of unstable angina?

Beta-blockers and ACE inhibitors.

p.3
Evaluation and Treatment of Myocardial Ischemia

What imaging technique is indicated to detect ischemic changes in asymptomatic individuals with multiple risk factors for coronary disease?

Stress radionucleotide imaging.

p.3
Evaluation and Treatment of Myocardial Ischemia

What ECG alterations are associated with ischemia?

ST segment depression, T wave inversion, and ST segment elevation.

p.5
Clinical Manifestations of Myocardial Ischemia

What are the clinical manifestations of unstable angina?

New-onset angina, angina occurring at rest, or angina increasing in severity or frequency, along with increased dyspnea, diaphoresis, and anxiety.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What happens when coronary blood flow is interrupted for an extended period?

Myocyte necrosis occurs, resulting in myocardial infarction (MI).

p.6
Acute Coronary Syndromes and Myocardial Infarction

What usually causes marked elevations in the ST segments on an ECG?

Transmural infarction.

p.1
Infection and Coronary Artery Disease (CAD)

Which microorganisms have been linked to an increased risk for CAD?

Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus have been linked to an increased risk for CAD.

p.6
Pathophysiology of Myocardial Ischemia

How quickly are myocardial oxygen reserves used after complete cessation of coronary flow?

Within about 8 seconds.

p.3
Evaluation and Treatment of Myocardial Ischemia

What diagnostic tool may be required during an angina attack in the absence of pain?

Electrocardiography (ECG).

p.3
Evaluation and Treatment of Myocardial Ischemia

What are the normal ECG deflections?

P wave, QRS complex, and T wave.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What leads to transient episodes of thrombotic vessel occlusion and vasoconstriction in unstable angina?

Fissuring or superficial erosion of the plaque.

p.5
Evaluation and Treatment of Myocardial Ischemia

What anticoagulants can be given for unstable angina?

Low-molecular-weight heparin or direct thrombin inhibitors like fondaparinux.

p.7
Pathophysiology of Myocardial Ischemia

What is released during myocardial ischemia and contributes to the pathogenesis of MI?

Angiotensin II.

p.6
Pathophysiology of Myocardial Ischemia

What happens to the myocardium after 8 to 10 seconds of decreased blood flow?

The affected myocardium becomes cyanotic and cooler.

p.1
Pathophysiology of Myocardial Ischemia

What happens if efficient exchange does not meet myocardial oxygen needs?

Healthy coronary arteries are able to dilate to increase the flow of oxygenated blood to the myocardium.

p.6
Pathophysiology of Myocardial Ischemia

How does norepinephrine affect blood sugar levels?

It elevates blood sugar levels through stimulation of liver and skeletal muscle cells.

p.1
Pathophysiology of Myocardial Ischemia

What happens to heart cells after several minutes of ischemia?

The heart cells lose the ability to contract, and cardiac output decreases.

p.4
Types of Angina: Stable and Prinzmetal

What are the different classes of drugs available to manage stable angina?

Nitrates, β-adrenergic receptor blockers, and calcium channel blockers.

p.2
Clinical Manifestations of Myocardial Ischemia

How is angina pectoris typically experienced?

As transient substernal chest discomfort, ranging from a sensation of heaviness or pressure to moderately severe pain.

p.4
Evaluation and Treatment of Myocardial Ischemia

What is percutaneous coronary intervention (PCI)?

A procedure where stenotic (narrowed) coronary vessels are dilated with a catheter.

p.2
Silent Ischemia and Mental Stress

How may angina present in individuals with autonomic nervous system dysfunction?

Angina may be mild, atypical, or even silent.

p.2
Types of Angina: Stable and Prinzmetal

When does the pain of Prinzmetal angina often occur?

At night during rapid eye movement sleep and may have a cyclic pattern of occurrence.

p.2
Silent Ischemia and Mental Stress

What may cause silent ischemia following surgical denervation?

Coronary artery bypass grafting (CABG) or cardiac transplantation.

p.3
Evaluation and Treatment of Myocardial Ischemia

What are characteristic signs of subendocardial ischemia frequently seen in angina?

Transient ST-segment depression and T-wave inversion.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What medications can help stabilize plaques and prevent rupture?

Statins, ACE inhibitors, and beta-blockers.

p.5
Acute Coronary Syndromes and Myocardial Infarction

How long does the thrombus occlude the vessel in unstable angina?

No more than 10 to 20 minutes.

p.5
Evaluation and Treatment of Myocardial Ischemia

What interventions are required for individuals with refractory angina or electrical/hemodynamic instability?

Immediate intervention with PCI or CABG.

p.5
Pathophysiology of Myocardial Ischemia

What happens if the thrombus breaks up before complete distal tissue necrosis has occurred?

The infarction will involve only the myocardium directly beneath the endocardium (subendocardial MI).

p.7
Pathophysiology of Myocardial Ischemia

How does angiotensin II contribute to the pathogenesis of MI?

By causing peripheral vasoconstriction and fluid retention, increasing myocardial work, and exacerbating the effects of the loss of myocyte contractility.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 18-24 hours after myocardial infarction?

Pale to gray-brown; slight pallor.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 10-14 days after myocardial infarction?

Weak, fibrotic scar tissue with beginning revascularization.

p.6
Acute Coronary Syndromes and Myocardial Infarction

What happens if a thrombus lodges permanently in a vessel?

The infarction will extend through the myocardium from endocardium to epicardium (transmural MI), resulting in severe cardiac dysfunction.

p.1
Infection and Coronary Artery Disease (CAD)

What is one hypothesis regarding systemic infection and vascular disease?

One hypothesis is that systemic infection results in increased inflammation of vessels and therefore contributes to vascular disease.

p.6
Pathophysiology of Myocardial Ischemia

What electrolyte disturbances accompany oxygen deprivation in myocardial cells?

Loss of potassium, calcium, and magnesium from cells.

p.1
Pathophysiology of Myocardial Ischemia

What are 'unstable' plaques prone to?

Unstable plaques are prone to ulceration or rupture.

p.6
Types of Angina: Stable and Prinzmetal

What is rest angina?

Angina occurring at rest and prolonged, usually >20 minutes.

p.2
Types of Angina: Stable and Prinzmetal

What causes unpredictable chest pain in the cardiovascular system?

Abnormal vasospasm of coronary vessels, resulting in Prinzmetal angina.

p.4
Types of Angina: Stable and Prinzmetal

Why should short-acting formulations of calcium channel blockers be used with caution?

Because of potentially harmful effects on cardiac contractility and heart rate.

p.3
Types of Angina: Stable and Prinzmetal

What ECG change is indicative of transmural ischemia and can be seen in individuals with Prinzmetal angina?

ST elevation.

p.5
Evaluation and Treatment of Myocardial Ischemia

What does the ECG commonly reveal during pain in unstable angina?

ST-segment depression and T-wave inversion that resolves as the pain is relieved.

p.7
Pathophysiology of Myocardial Ischemia

What results from the necrosis of myocardial tissue?

The release of certain intracellular enzymes through the damaged cell membranes into the interstitial spaces.

p.7
Evaluation and Treatment of Myocardial Ischemia

What may an increased understanding of the apoptotic pathway of MI lead to?

New therapies aimed at limiting infarct size.

p.6
Pathophysiology of Myocardial Ischemia

How long can cardiac cells withstand ischemic conditions before cellular death occurs?

About 20 minutes.

p.1
Impact of Air Pollution on Heart Health

What do toxins in pollution contribute to?

Toxins in pollution contribute to macrophage activation, oxidation of LDL, thrombosis, and inflammation of vessel walls.

p.6
Pathophysiology of Myocardial Ischemia

What do ischemic myocardial cells release that predisposes individuals to serious imbalances of sympathetic and parasympathetic function?

Catecholamines (epinephrine and norepinephrine).

p.1
Pathophysiology of Myocardial Ischemia

What can thrombus formation suddenly cause?

Thrombus formation can suddenly cut off blood supply to the heart muscle, resulting in acute myocardial ischemia.

p.6
Types of Angina: Stable and Prinzmetal

What is increasing angina?

Previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold (increased by ≥ 1 CCS class to at least CCS class III severity).

p.4
Types of Angina: Stable and Prinzmetal

What is the first-line therapy to reduce myocardial oxygen requirements during physical exertion?

β-Adrenergic receptor blockers.

p.4
Evaluation and Treatment of Myocardial Ischemia

How can the risk of restenosis after PCI be reduced?

By placing a coronary stent.

p.2
Types of Angina: Stable and Prinzmetal

What causes the pain in Prinzmetal angina?

Vasospasm of one or more major coronary arteries with or without associated atherosclerosis.

p.2
Evaluation and Treatment of Myocardial Ischemia

How are most individuals with Prinzmetal angina treated?

With vasodilators, and the overall prognosis is good.

p.2
Silent Ischemia and Mental Stress

When may silent ischemia occur in some individuals?

During mental stress.

p.3
Evaluation and Treatment of Myocardial Ischemia

What is the primary aim of therapy for myocardial ischemia and angina?

To increase delivery of oxygen by improving coronary artery blood flow and to reduce myocardial oxygen consumption.

p.5
Evaluation and Treatment of Myocardial Ischemia

What additional antithrombotic therapies may be indicated for unstable angina?

Clopidogrel or IIb/IIIa platelet receptor antagonists.

p.7
Pathophysiology of Myocardial Ischemia

What does reperfusion injury involve?

The release of toxic oxygen radicals, calcium flux, and pH changes.

p.1
Adipokines and Cardiovascular Health

How do weight loss and exercise affect adipokine levels?

Weight loss and exercise improve adipokine levels and are correlated with improved cardiovascular risk.

p.1
Infection and Coronary Artery Disease (CAD)

What other condition has been linked to an increased risk for CAD?

Periodontal disease has been linked to an increased risk for CAD.

p.6
Pathophysiology of Myocardial Ischemia

What accumulates in myocardial tissues due to poor buffering capabilities and sensitivity to low cellular pH?

Hydrogen ions and lactic acid.

p.1
Pathophysiology of Myocardial Ischemia

What is the most common cause of decreased coronary blood flow and resultant myocardial ischemia?

The formation of atherosclerotic plaques in the coronary circulation is the most common cause.

p.6
Acute Coronary Syndromes and Myocardial Infarction

What is shown in Figure 32-21A?

Plaque disruption with the cap of the lipid-rich plaque torn and the formation of a thrombus mostly inside the plaque.

p.1
Pathophysiology of Myocardial Ischemia

What happens if blood flow is restored within 20 minutes?

Aerobic metabolism resumes, contractility is restored, and cellular repair begins.

p.4
Types of Angina: Stable and Prinzmetal

What medications are indicated for plaque stabilization, regression, and prevention of clotting in individuals with stable angina?

Statins, ACE inhibitors or receptor blockers, and antithrombotics.

p.4
Evaluation and Treatment of Myocardial Ischemia

What surgical procedure is used to treat severe CAD?

Coronary artery bypass grafting (CABG), usually using the saphenous vein from the lower leg.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What results from prolonged ischemia causing irreversible damage to the heart muscle?

Myocardial infarction (MI).

p.4
Acute Coronary Syndromes and Myocardial Infarction

What results from platelet activation during plaque disruption?

Release of coagulants and exposure of platelet glycoprotein IIb/IIIa surface receptors, leading to further platelet aggregation and adherence.

p.2
Silent Ischemia and Mental Stress

What has mental stress been linked to in relation to silent ischemia?

Increased markers of inflammation, decreased activity of vasodilators, and a hypercoagulable state.

p.2
Evaluation and Treatment of Myocardial Ischemia

What may a physical examination of an individual experiencing myocardial ischemia disclose?

Tachycardia, extra heart sounds (gallops or murmurs), and pulmonary congestion.

p.3
Silent Ischemia and Mental Stress

What are the potential cardiac effects of acute mental stress?

Myocardial ischemia, potentially fatal dysrhythmia, plaque rupture, or coronary thrombosis.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What are other causes of myocardial infarction besides atherosclerotic CAD?

Coronary spasm and coronary artery embolism.

p.7
Evaluation and Treatment of Myocardial Ischemia

What are some therapies being explored to reduce reperfusion injury?

Endovascular cooling, adenosine, atrial natriuretic peptide, cyclosporine, nicorandil, and incretins.

p.7
Pathophysiology of Myocardial Ischemia

What happens after about 20 minutes of myocardial ischemia?

Irreversible hypoxic injury causes cellular death and tissue necrosis.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 4-10 days after myocardial infarction?

Area soft, with fatty changes in center, regions of hemorrhage in infarcted area.

p.6
Pathophysiology of Myocardial Ischemia

What effect does acidosis have on the myocardium?

It may make the myocardium more vulnerable to the damaging effects of lysosomal enzymes and may suppress impulse conduction and contractile function, leading to heart failure.

p.1
Pathophysiology of Myocardial Ischemia

What happens as atherosclerotic plaques increase in size?

They may partially occlude the vessel lumina, limiting coronary flow and causing ischemia especially during exercise.

p.6
Acute Coronary Syndromes and Myocardial Infarction

What is shown in Figure 32-21B?

A myocardial infarction that is 6 days old with a yellow and necrotic center and a hemorrhagic red rim.

p.1
Clinical Manifestations of Myocardial Ischemia

How do individuals with reversible myocardial ischemia present clinically?

Individuals with reversible myocardial ischemia present clinically in several ways.

p.4
Types of Angina: Stable and Prinzmetal

What is the mechanism of action of calcium channel blockers in reducing myocardial oxygen demand?

They decrease the influx of calcium into myocardial and vascular smooth muscle cells and modify the pacemaker activity of the sinoatrial (SA) node and conduction properties of the atrioventricular (AV) node.

p.4
Evaluation and Treatment of Myocardial Ischemia

When is coronary revascularization indicated?

For individuals who do not respond adequately to antianginal drugs or who have high-risk atherosclerotic lesions.

p.4
Evaluation and Treatment of Myocardial Ischemia

What is minimally invasive direct coronary artery bypass (MIDCAB)?

A modified CABG procedure with much less surgical morbidity and more rapid recovery.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What are the two types of myocardial infarction (MI)?

Non–ST-elevation MI (non-STEMI) and ST-elevation MI (STEMI).

p.4
Acute Coronary Syndromes and Myocardial Infarction

What can exacerbate vessel obstruction during thrombus formation?

Release of vasoconstrictors such as thromboxane A2 and endothelin.

p.3
Evaluation and Treatment of Myocardial Ischemia

What imaging techniques are used to document coronary obstruction but cannot detect unstable plaques?

Radioisotope imaging with thallium-201 and stress echocardiography.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What is unstable angina?

A form of acute coronary syndrome that results in reversible myocardial ischemia.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What percentage of people with unstable angina progress to MI or death within hours to days?

Approximately 20%.

p.7
Pathophysiology of Myocardial Ischemia

What surrounds the infarcted myocardium?

A zone of hypoxic injury, which may progress to necrosis, undergo remodeling, or return to normal.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 2-4 days after myocardial infarction?

Visible necrosis: yellow-brown in center and hyperemic around edges.

p.6
Pathophysiology of Myocardial Ischemia

How quickly can ECG changes be visible after hypoxia begins?

After only 30 to 60 seconds.

p.6
Pathophysiology of Myocardial Ischemia

What percentage of the total myocardial energy requirement can glycolysis supply?

65% to 70%.

p.1
Pathophysiology of Myocardial Ischemia

What other causes can lead to decreased blood and oxygen delivery to the myocardium?

Other causes include coronary spasm, hypotension, dysrhythmias, and decreased oxygen-carrying capacity of the blood (anemia, hypoxemia).

p.1
Pathophysiology of Myocardial Ischemia

What occurs if coronary artery occlusion persists beyond 20 minutes?

Myocardial infarction (MI) occurs.

p.2
Types of Angina: Stable and Prinzmetal

What happens to affected vessels in stable angina during increased myocardial demand?

They cannot dilate in response to increased myocardial demand associated with physical exertion or emotional stress.

p.2
Clinical Manifestations of Myocardial Ischemia

What causes the pain in angina pectoris?

The buildup of lactic acid or abnormal stretching of the ischemic myocardium that irritates myocardial nerve fibers.

p.2
Evaluation and Treatment of Myocardial Ischemia

What does a lack of relief from anginal pain indicate?

An individual may be developing infarction.

p.2
Types of Angina: Stable and Prinzmetal

What other causes may lead to Prinzmetal angina?

Altered calcium channel function in arterial smooth muscle and endothelial dysfunction with release of inflammatory mediators.

p.2
Silent Ischemia and Mental Stress

Who is more likely to experience silent ischemia and atypical symptoms?

Women.

p.2
Evaluation and Treatment of Myocardial Ischemia

What do the presence of xanthelasmas or arcus senilis suggest?

Dyslipidemia and possible atherosclerosis.

p.3
Evaluation and Treatment of Myocardial Ischemia

What is the modality of choice for the diagnosis of myocardial ischemia?

Single-photon emission computed tomography (SPECT).

p.5
Evaluation and Treatment of Myocardial Ischemia

What do serum cardiac biomarkers indicate in unstable angina?

They remain normal.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What is the most common cause of myocardial infarction?

Atherosclerotic coronary artery disease (CAD).

p.5
Acute Coronary Syndromes and Myocardial Infarction

Why is it important to recognize non-STEMI?

Because recurrent clot formation on the disrupted atherosclerotic plaque can occur.

p.7
Pathophysiology of Myocardial Ischemia

When do gross tissue changes in the area of infarction become apparent?

Several hours after MI, despite almost immediate onset of ECG changes.

p.1
Adipokines and Cardiovascular Health

What are the effects of anti-inflammatory, insulin-sensitizing enhancement of nitric oxide generation?

They attenuate reactive oxygen species production in endothelial cells and reduce vascular smooth muscle cell proliferation.

p.1
Infection and Coronary Artery Disease (CAD)

Have antibiotics been effective in preventing and treating CAD?

The use of antibiotics for the prevention and treatment of CAD has not yielded consistently positive results.

p.6
Pathophysiology of Myocardial Ischemia

What happens to myocardial cells deprived of necessary oxygen and nutrients?

They lose contractility, diminishing the heart’s pumping ability.

p.1
Pathophysiology of Myocardial Ischemia

What results from the ulceration or rupture of plaques?

Underlying tissues of the vessel wall are exposed, resulting in platelet adhesion and thrombus formation.

p.1
Pathophysiology of Myocardial Ischemia

What abnormalities can ischemia cause?

Ischemia can cause conduction abnormalities that lead to changes in the electrocardiogram and may initiate dysrhythmias.

p.4
Types of Angina: Stable and Prinzmetal

How do nitrates improve coronary blood flow and reduce myocardial demand?

By decreasing peripheral vascular resistance and venous return to the heart (preload), thereby reducing cardiac workload.

p.2
Clinical Manifestations of Myocardial Ischemia

How do individuals often describe the sensation of angina pectoris?

By clenching a fist over the left sternal border.

p.4
Evaluation and Treatment of Myocardial Ischemia

What is the major complication of PCI?

Restenosis of the artery.

p.2
Types of Angina: Stable and Prinzmetal

What is Prinzmetal angina?

Chest pain attributable to transient ischemia of the myocardium that occurs unpredictably and almost exclusively at rest.

p.2
Types of Angina: Stable and Prinzmetal

What may happen if the spasm in Prinzmetal angina persists long enough?

Infarction or serious dysrhythmias may occur.

p.2
Silent Ischemia and Mental Stress

How is screening for silent ischemia conducted?

Based on the presence of risk factors and most often detected using stress radionucleotide imaging.

p.3
Evaluation and Treatment of Myocardial Ischemia

What percentage of individuals with angina have nondiagnostic ECG tracings?

Approximately 30%.

p.5
Evaluation and Treatment of Myocardial Ischemia

What might a physical examination reveal in a person with unstable angina?

Evidence of ischemic myocardial dysfunction such as tachycardia or pulmonary congestion.

p.5
Acute Coronary Syndromes and Myocardial Infarction

What are the two major types of myocardial infarction pathologically?

Subendocardial infarction and transmural infarction.

p.5
Evaluation and Treatment of Myocardial Ischemia

How does subendocardial MI usually present on an ECG?

With ST depression and T-wave inversion.

p.7
Pathophysiology of Myocardial Ischemia

What recent evidence has been found regarding myocardial tissue destruction?

Myocardial tissue is also destroyed by the tightly controlled process of apoptosis.

p.6
Acute Coronary Syndromes and Myocardial Infarction

What is the clinical significance of identifying individuals with STEMI?

They are at highest risk for serious complications and require immediate intervention.

p.6
Pathophysiology of Myocardial Ischemia

What is ischemic preconditioning?

A process where previous recurrent episodes of myocardial ischemia result in myocyte adaptation to oxygen deprivation and preservation of myocardium.

p.6
Pathophysiology of Myocardial Ischemia

What happens to glycogen stores during anaerobic metabolism?

Glycogen stores decrease.

p.1
Pathophysiology of Myocardial Ischemia

What are common causes of increased myocardial demand for blood?

Common causes include tachycardia, exercise, hypertension (hypertrophy), and valvular disease.

p.6
Pathophysiology of Myocardial Ischemia

Why is careful glucose monitoring and control essential after an MI?

Because hyperglycemia is associated with an increased risk of death.

p.6
Types of Angina: Stable and Prinzmetal

How do individuals with non-ST-elevation myocardial infarction (non-STEMI) usually present?

With angina at rest.

p.2
Types of Angina: Stable and Prinzmetal

What causes stable angina?

Gradual luminal narrowing and hardening of the arterial walls.

p.2
Clinical Manifestations of Myocardial Ischemia

What may the discomfort of angina pectoris be mistaken for?

Indigestion.

p.4
Evaluation and Treatment of Myocardial Ischemia

What treatments can improve outcomes after stenting?

Antithrombotic treatments such as aspirin, clopidogrel, or glycoprotein IIb/IIIa receptor antagonists.

p.2
Types of Angina: Stable and Prinzmetal

What factors may contribute to Prinzmetal angina?

Decreased vagal activity, hyperactivity of the sympathetic nervous system, and decreased nitric oxide activity.

p.2
Silent Ischemia and Mental Stress

What are the nonspecific symptoms associated with silent ischemia?

Fatigue, dyspnea, or feeling of unease.

p.3
Coronary Artery Calcification (CAC) and Imaging Techniques

What imaging methods are used for the evaluation of atherosclerotic plaques in coronary arteries?

CT with and without angiography, MRI, or intravascular ultrasound.

p.5
Evaluation and Treatment of Myocardial Ischemia

What is the immediate management required for unstable angina?

Immediate hospitalization with administration of oxygen, aspirin, nitrates, and morphine if pain is still present.

p.5
Acute Coronary Syndromes and Myocardial Infarction

How is myocardial infarction clinically categorized?

As non-STEMI or STEMI.

p.7
Pathophysiology of Myocardial Ischemia

What can exacerbate ischemic injury once blood flow is restored?

Reperfusion injury.

p.7
Pathophysiology of Myocardial Ischemia

What local effects does angiotensin II have during myocardial ischemia?

It acts as a growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts; promotes catecholamine release; and causes coronary artery spasm.

p.7
Pathophysiology of Myocardial Ischemia

What changes result from MI in cardiac tissues?

Structural and functional changes.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 6 weeks after myocardial infarction?

Scarring usually complete.

p.1
Adipokines and Cardiovascular Health

What is resistin linked to?

Resistin is linked to inflammation, endothelial dysfunction, thrombosis, and smooth muscle cell dysfunction.

p.1
Impact of Air Pollution on Heart Health

What is strongly correlated with coronary risk?

Exposure to air pollution, especially roadway exposures, is strongly correlated with coronary risk.

p.1
Pathophysiology of Myocardial Ischemia

When does myocardial ischemia develop?

Myocardial ischemia develops if the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients.

p.6
Pathophysiology of Myocardial Ischemia

When is hyperglycemia noted after an acute MI?

Approximately 72 hours after an acute MI.

p.1
Pathophysiology of Myocardial Ischemia

What processes take over during ischemia?

Anaerobic processes take over, and lactic acid accumulates.

p.2
Clinical Manifestations of Myocardial Ischemia

What is angina pectoris?

Chest pain caused by myocardial ischemia.

p.4
Types of Angina: Stable and Prinzmetal

Do antianginal medications reverse the atherosclerotic process?

No, they do not reverse the atherosclerotic process.

p.2
Clinical Manifestations of Myocardial Ischemia

What symptoms may be associated with anginal pain?

Pallor, diaphoresis, and dyspnea.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What causes acute coronary syndromes?

Sudden coronary obstruction caused by thrombus formation over a ruptured or ulcerated atherosclerotic plaque.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What factors contribute to plaque disruption?

Shear forces, inflammation with release of multiple inflammatory mediators, secretion of macrophage-derived degradative enzymes, and apoptosis of cells at the edges of the lesions.

p.2
Silent Ischemia and Mental Stress

Why is the detection of silent ischemia important?

It is an indicator of increased risk for serious cardiovascular disease (CVD) events, and aggressive treatment may be indicated.

p.5
Pathophysiology of Myocardial Ischemia

What is the pathophysiology of myocardial infarction?

Plaque progression, disruption, and subsequent clot formation, with the thrombus occluding the vessel for a prolonged period, leading to myocyte necrosis and death.

p.7
Pathophysiology of Myocardial Ischemia

What changes occur in cardiac tissue surrounding the area of infarction?

Pathophysiologic changes.

p.1
Adipokines and Cardiovascular Health

What role do adipokine changes in perivascular adipose cells play?

Adipokine changes in perivascular adipose cells may play a significant role in metabolic and vascular disorders.

p.1
Coronary Artery Calcification (CAC) and Imaging Techniques

How can coronary risk related to changes in vessel walls be assessed?

Coronary risk can be assessed using various types of vascular imaging techniques such as CAC detected by CT scanning and CIMT detected by ultrasonography.

p.6
Pathophysiology of Myocardial Ischemia

What effect do catecholamines have on plasma concentrations of free fatty acids and glycerol?

They cause plasma concentrations of free fatty acids and glycerol to rise within 1 hour after onset of acute MI.

p.1
Pathophysiology of Myocardial Ischemia

What happens if vessel obstruction cannot be reversed rapidly?

Ischemia will progress to infarction.

p.1
Pathophysiology of Myocardial Ischemia

How long do cardiac cells remain viable under ischemic conditions?

Cardiac cells remain viable for approximately 20 minutes under ischemic conditions.

p.4
Types of Angina: Stable and Prinzmetal

How do beta-blockers enhance oxygen delivery to the heart?

By reducing heart rate, which provides additional diastolic filling time for coronary perfusion.

p.2
Evaluation and Treatment of Myocardial Ischemia

How is anginal pain usually relieved?

By rest and nitrates.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What is unstable angina?

The result of reversible myocardial ischemia and a harbinger of impending infarction.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What happens when the plaque substrate is exposed?

It activates the clotting cascade.

p.2
Evaluation and Treatment of Myocardial Ischemia

What is a critical tool for diagnosing myocardial ischemia?

Electrocardiography (ECG).

p.5
Pathophysiology of Myocardial Ischemia

What determines the size and character of a myocardial infarction?

The duration of ischemia.

p.7
Pathophysiology of Myocardial Ischemia

What causes a sustained opening of mitochondrial permeability transition pores (mPTP) during reperfusion injury?

The release of toxic oxygen radicals, calcium flux, and pH changes.

p.7
Pathophysiology of Myocardial Ischemia

How are the enzymes released from necrotic myocardial tissue detected?

They are picked up by the lymphatics and transported into the bloodstream, where they can be detected by serologic tests.

p.7
Pathophysiology of Myocardial Ischemia

What are the tissue changes 6-12 hours after myocardial infarction?

No gross changes; subcellular cyanosis with decreased temperature.

p.6
Pathophysiology of Myocardial Ischemia

Can metabolically altered and nonfunctional cardiac cells remain viable if blood flow returns within a certain time?

Yes, they can remain viable if blood flow returns within 20 minutes.

p.1
Pathophysiology of Myocardial Ischemia

What do the coronary arteries normally supply?

The coronary arteries normally supply blood flow sufficient to meet the demands of the myocardium as it labors under varying workloads.

p.6
Pathophysiology of Myocardial Ischemia

What harmful effect can excessive levels of free fatty acids have on cell membranes?

They can have a harmful detergent effect.

p.1
Pathophysiology of Myocardial Ischemia

How quickly do myocardial cells become ischemic after coronary occlusion?

Myocardial cells become ischemic within 10 seconds of coronary occlusion.

p.2
Types of Angina: Stable and Prinzmetal

What is the result of obstruction in the cardiovascular system?

Recurrent predictable chest pain called stable angina.

p.2
Types of Angina: Stable and Prinzmetal

What is the result if myocardial demand is decreased in stable angina?

No necrosis of myocardial cells results.

p.2
Clinical Manifestations of Myocardial Ischemia

How may myocardial ischemia present in women?

With atypical chest pain, palpitations, sense of unease, and severe fatigue.

p.2
Types of Angina: Stable and Prinzmetal

What serum markers may be elevated in individuals with Prinzmetal angina?

CRP and IL-6.

p.2
Silent Ischemia and Mental Stress

What abnormalities have been implicated in autonomic dysfunction in diabetes mellitus?

Global or regional abnormalities in left ventricular sympathetic afferent innervation.

p.1
Pathophysiology of Myocardial Ischemia

What impairs blood flow sufficiently to hamper cellular metabolism?

Narrowing of a major coronary artery by more than 50% impairs blood flow sufficiently to hamper cellular metabolism under conditions of increased myocardial demand.

p.6
Pathophysiology of Myocardial Ischemia

What is the effect of norepinephrine on pancreatic B-cell activity?

It suppresses pancreatic B-cell activity, reducing insulin secretion and elevating blood glucose further.

p.6
Types of Angina: Stable and Prinzmetal

What is new-onset angina?

New-onset angina of at least Canadian Cardiovascular Society (CCS) class III severity.

p.2
Silent Ischemia and Mental Stress

What is myocardial ischemia that does not cause detectable symptoms called?

Silent ischemia.

p.4
Types of Angina: Stable and Prinzmetal

What is the benefit of combining nitrates, beta-blockers, and calcium antagonists in treating ischemic heart disease?

They may provide dramatic relief from clinical manifestations, improve quality of life, and make more invasive interventions unnecessary.

p.2
Clinical Manifestations of Myocardial Ischemia

What are the possible locations and radiation patterns of anginal pain?

Pain may radiate to the neck, lower jaw, left arm, left shoulder, back, or down the right arm.

p.4
Evaluation and Treatment of Myocardial Ischemia

What new drugs are being evaluated for the medical management of myocardial ischemic syndromes?

Ranolazine, trimetazidine, nicorandil, and ivabradine.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What is an 'unstable' atherosclerotic plaque?

A plaque prone to rupture with a core rich in deposited oxidized LDL and a thin fibrous cap.

p.2
Silent Ischemia and Mental Stress

What may cause silent ischemia following ischemic local nerve injury?

Myocardial infarction (MI).

p.2
Silent Ischemia and Mental Stress

What is the purpose of further research into brain-heart pathways?

To better elucidate appropriate interventions.

p.2
Clinical Manifestations of Myocardial Ischemia

Where do the afferent sympathetic fibers that cause anginal pain enter the spinal cord?

From levels C3 to T4.

p.4
Evaluation and Treatment of Myocardial Ischemia

What investigational therapies are being explored for refractory angina?

Transmyocardial laser revascularization (TMR), gene therapy for myocardial angiogenesis, spinal cord stimulation, laser revascularization, and percutaneous in situ coronary venous arterialization.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What can result from any of the acute coronary syndromes?

Sudden cardiac death.

p.4
Acute Coronary Syndromes and Myocardial Infarction

What can happen if the thrombus breaks up before permanent myocyte damage occurs?

Unstable angina.

p.2
Silent Ischemia and Mental Stress

What has stress management been associated with in men?

A reduction in CAD events.

p.2
Evaluation and Treatment of Myocardial Ischemia

What does the presence of peripheral or carotid arterial bruits suggest?

Probable atherosclerotic disease and increases the likelihood that CAD is present.

Study Smarter, Not Harder
Study Smarter, Not Harder