Cardio - Mechanisms of Disease - Heart Failure; Ischemic Heart Disease Flashcards

1
Q

Name some of the many causes of congestive heart failure.

A

Ischemic heart disease;

chronic hypertension;

cardiomyopathies;

infections;

toxins;

valvular disease;

prolonged arrhythmias

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2
Q

Systolic heart failure is associated with an S__ heart sound and _________ ventricles.

A

Systolic heart failure is associated with an S3 heart sound and dilated ventricles.

(3 = SYS-tolic

4 = DIAS-tolic)

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3
Q

Diastolic heart failure is associated with an S__ heart sound and _________ ventricles.

A

Diastolic heart failure is associated with an S4 heart sound and hypertrophic ventricles.

(4 = DIAS-tolic

3 = SYS-tolic)

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4
Q

_________ heart failure is associated with an S3 heart sound and _________ ventricles.

A

Systolic heart failure is associated with an S3 heart sound and dilated ventricles.

(3 = SYS-tolic

4 = DIAS-tolic)

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5
Q

_________ heart failure is associated with an S4 heart sound and _________ ventricles.

A

Diastolic heart failure is associated with an S4 heart sound and hypertrophic ventricles.

(4 = DIAS-tolic

3 = SYS-tolic)

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6
Q

Systolic heart failure is also known as heart failure with _________ ejection fraction (HF__EF).

A

Systolic heart failure is also known as heart failure with reduced ejection fraction (HFrEF).

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7
Q

Diastolic heart failure is also known as heart failure with _________ ejection fraction (HF__EF).

A

Diastolic heart failure is also known as heart failure with preserved ejection fraction (HFpEF).

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8
Q

Name three categories of compensatory mechanisms used by the heart to prevent complete failure:

Ventricular ___________

Neuro_________ activation

___________-__________ mechanism

A

Name three categories of compensatory mechanisms used by the heart to prevent complete failure:

Ventricular remodeling

Neurohormonal activation

Frank-Starling mechanism

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9
Q

What are the two main forms of ventricular remodeling?

A
  1. Myocardial hypertrophy
  2. Chamber dilatation
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10
Q

The hypertrophy or dilatation seen in congestive heart failure are compensatory mechanisms used to decrease what?

A

Ventricular wall tension

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11
Q

Concentric myocardial hypertrophy is to place the myocytes in _________.

A

Concentric myocardial hypertrophy is to place the myocytes in parallel.

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12
Q

Eccentric myocardial hypertrophy is to place the myocytes in ______.

A

Eccentric myocardial hypertrophy is to place the myocytes in series.

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13
Q

________ overload leads to concentric cardiac hypertrophy.

A

Pressure overload leads to concentric cardiac hypertrophy.

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14
Q

________ overload leads to eccentric cardiac hypertrophy.

A

Volume overload leads to eccentric cardiac hypertrophy.

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15
Q

Which form of cardiac hypertrophy (eccentric or concentric) sometimes occurs under normal physiologic conditions?

A

Eccentric

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16
Q

Via what two mechanisms can cardiac hypertrophy lead to myocardial ischemia?

A
  1. Increased O2 requirement
  2. Myocardial growth compresses the coronary arteries
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17
Q

Ventricular remodeling typically results in the heart taking on a more __________ shape.

A

Ventricular remodeling typically results in the heart taking on a more globular (spherical) shape.

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18
Q

The Law of LaPlace indicates that wall tension is proportional to what two internal chamber factors?

A

(1) radius (r)
(2) pressure (P)

(Tension = P*r /2h)

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19
Q

The Law of LaPlace indicates that wall tension is inversely proportional to what factor?

A

Wall thickness (h)

(Tension = P*r /2h)

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20
Q

Is left ventricular hypertrophy more associated with systolic or diastolic heart failure?

A

Diastolic

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21
Q

Is ischemic heart disease more associated with systolic or diastolic heart failure?

A

Systolic

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22
Q

Is cardiac fibrosis/amyloidosis more associated with systolic or diastolic heart failure?

A

Diastolic

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23
Q

Is hypertension more associated with systolic or diastolic heart failure?

A

Systolic

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24
Q

Which form(s) of natriuretic peptide arise(s) from the atria?

Which form(s) of natriuretic peptide arise(s) from the CNS?

A

ANP, BNP;

CNP

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25
Q

What type of nuclei are seen in hypertrophied cardiomyocytes?

A

Boxcar nuclei

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26
Q

Left-to-right shunting can increase risk of ______-sided heart failure.

A

Left-to-right shunting can increase risk of right-sided heart failure.

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27
Q

Describe the appearance of the alveolar pink edematous fluid seen in cases of left heart failure.

A
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28
Q

Describe the appearance of the hemosiderin-laden alveolar macrophages seen in cases of left heart failure.

A
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29
Q

Describe the nutmeg liver seen in cases of right heart failure.

A
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30
Q

The nutmeg liver seen in right heart failure is a result of __________ deposition around the _______ tubular focus in the liver due to passive congestion.

A

The nutmeg liver seen in right heart failure is a result of hemosiderin deposition around the central tubular focus in the liver due to passive congestion.

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31
Q

Cardiac tumors are almost always _________ (primary/secondary).

A

Cardiac tumors are almost always secondary (malignant metastases).

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32
Q

Metastases to the heart typically come from what primary malignancies?

A

Lymphoma;

melanoma;

breast

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33
Q

Primary cardiac tumors are typically benign, of which ____% are myxomas.

A

Primary cardiac tumors are typically benign, of which 50% are myxomas.

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34
Q

50% of cardiac rhabdomyomas are associated with what condition?

A

Tuberous sclerosis

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35
Q

Cardiac myxomas are typically attached to what structure?

A

The interatrial septum

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36
Q

Cardiac fibromas are typically _______al.

A

Cardiac fibromas are typically congenital.

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37
Q

Cardiac lipomas are most common in what patient population?

A

Obese adults

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38
Q

Cardiac papillary elastomas are most common in what patient population?

A

Older adults

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39
Q

Cardiac _________ are benign proliferations of blood vessels.

A

Cardiac hemangiomas are benign proliferations of blood vessels.

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40
Q

What is the most common primary cardiac malignancy?

A

Angiosarcoma

(then rhabdomyosarcoma, then leiomyosarcoma)

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41
Q

Describe the histology of myxomas.

A

Stellate or globular myxoma cells with abundant eosinophilic cytoplasm; placed in an abundant mucopolysaccharide ground substance

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42
Q

True/False.

For all intents and purposes, ischemic heart disease and coronary artery disease are the same condition.

A

True.

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43
Q

90% of cases of coronary artery disease / ischemic heart disease are caused by what?

A

Coronary artery atherosclerosis

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44
Q

Myocardial ischemia is defined as a mismatch between oxygen _______ and oxygen _______.

A

Myocardial ischemia is defined as a mismatch between oxygen supply and oxygen demand.

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45
Q

Myocardial oxygen demand is mainly dependent on what factors?

A

Contractility;

wall tension

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46
Q

A pressure-flow graph shows that flow ________s as the pressure decreases (as in cases of stenosis).

A

A pressure-flow graph shows that flow decreases as the pressure decreases (as in cases of stenosis).

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47
Q

What is the threshold of coronary artery occlusion that can lead to angina pectoris?

A

70% occlusion

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48
Q

A coronary artery 70% occlusion results in a pressure drop of ____ mmHg.

A coronary artery 90% occlusion results in a pressure drop of ____ mmHg.

A

A coronary artery 70% occlusion results in a pressure drop of 45 mmHg.

A coronary artery 90% occlusion results in a pressure drop of 55 mmHg.

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49
Q

The coronary artery oxygen supply is dependent on __________ (systolic/diastolic) pressures.

A

The coronary artery oxygen supply is dependent on diastolic pressures.

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50
Q

What equation represents the relationship between pressure and flow?

A

Flow = pressure / resistance

(Think Ohm’s law — Voltage = Current * Resistance — V = IR)

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51
Q

Name three acute coronary syndromes.

A
  1. Angina pectoris
  2. Sudden cardiac death
  3. Myocardial infarction
52
Q

What are the three main types of angina pectoris?

A
  1. Stable (classical)
  2. Unstable (crescendo)
  3. Printzmetal (variant)
53
Q

Stable angina typically requires ≥ ___% occlusion of coronary vessels.

A

Stable angina typically requires ≥ 75% occlusion of coronary vessels.

54
Q

Unstable angina typically requires ≥ ___% occlusion of coronary vessels.

A

Unstable angina typically requires ≥ 90% occlusion of coronary vessels.

55
Q

Printzmetal angina is associated with changes in which of the following?

Activity level

Heart rate

Blood pressure

A

None!

Coronary artery vasospasm

56
Q

What type of angina typically occurs in young females, is associated with cigarette/cocaine use, occurs in the early morning hours, and is associated with migraines and Raynaud’s phenomenon?

A

Printzmetal

57
Q

What type of clinical/laboratory results are seen in Printzmetal angina?

A

Transient ST-segment elevation

(and subsequently found to not have high grade coronary stenosis at coronary arteriography)

58
Q

Describe the therapeutic goals in treating Printzmetal angina.

A
  1. Treat with nitroglycerin and/or calcium channel blockers (vasodilators)
  2. Eliminate risk factors; e.g. smoking and/or drug abuse
59
Q

What are the most dangerous clinical outcomes associated with Printzmetal angina?

A

Myocardial infarction and life-threatening arrhythmias

(25% of untreated cases)

60
Q

___ - ___ minutes of severe ischemia are necessary for irreversible necrosis of cardiac myocytes.

A

20 - 40 minutes of severe ischemia are necessary for irreversible necrosis of cardiac myocytes.

61
Q

_________ cardiomyocytes use the most energy and will die first in cases of infarction.

A

Endocardial cardiomyocytes use the most energy and will die first in cases of infarction.

62
Q

Describe the way myocardial infarctions spread through the heart layers.

A
63
Q

Which is more damaging, (1) myocardial ischemia or (2) the reperfusion injury following administration of thrombolytics?

A

Myocardial ischemia

64
Q

Cardiogenic shock is most likely after the death of ___% of cardiomyocytes.

A

Cardiogenic shock is most likely after the death of 40% of cardiomyocytes.

65
Q

True/False.

More myocardial death leads to more serum troponin I.

(Directly proportional)

A

True.

66
Q

Via what mechanism does exercise/stress cause angina pectoris in patients with coronary artery disease?

A

The stenotic vessel fails to meet the increased myocardial oxygen demand

67
Q

Angina is characterized by __________ (reversible/irreversible) myocardial damage.

A

Angina is characterized by reversible myocardial damage.

68
Q

The coronary arteries can typically supply all the needed oxygen to the myocardium until atherosclerotic plaques occlude a minimum of ___% of the vessel.

A

The coronary arteries can typically supply all the needed oxygen to the myocardium until atherosclerotic plaques occlude a minimum of 70% of the vessel.

69
Q

An angina episode typically lasts ≤ ___ minutes.

A

An angina episode typically lasts ≤ 20 minutes.

70
Q

Why is it valuable to know that angina episodes don’t last any longer than 20 minutes?

A

That is the extent to which myocardial ischemia/damage is completely reversible

(after 20 minutes, this constitutes an AMI as the damage becomes irreversible)

71
Q

What is the technical term for heavy sweating (often as a result of AMI)?

A

Diaphoresis

72
Q

Why does stable angina present with ST segment depressions?

A

The subendocarium is farthest from the coronary arteries, hence it is damaged by ischemic conditions first

(ST depression indicates subendocardial ischemia)

73
Q

________ angina is an example of subendocardial ischemia.

A

Stable angina is an example of subendocardial ischemia.

74
Q

True/False.

As opposed to stable angina, unstable angina represents irreversible damage to myocardial tissue.

A

False.

Unstable angina represents reversible damage to myocardial tissue.

75
Q

What typically causes episodes of unstable angina?

A

Plaque rupture

(+ thrombosis and incomplete resulting vessel occlusion)

76
Q

Atherosclerotic plaques usually rupture along which portion of the plaque bulge?

A

The plaque neck

(the junction of the plaque with normal intima)

77
Q

Stable angina is characterized by ST segment _____________.

Unstable angina is characterized by ST segment _____________.

A

Stable angina is characterized by ST segment depression.

Unstable angina is characterized by ST segment depression.

(Both examples of subendocardial ischemia)

78
Q

Unstable angina results from plaque rupture and __________ occlusion of a coronary vessel.

AMIs results from plaque rupture and __________ occlusion of a coronary vessel.

A

Unstable angina results from plaque rupture and incomplete occlusion of a coronary vessel.

AMIs results from plaque rupture and complete occlusion of a coronary vessel.

79
Q

The S/Sy associated with an AMI ______ (are/are not) reversed by administration of nitroglycerin.

A

The S/Sy associated with an AMI are not reversed by administration of nitroglycerin.

80
Q

In descending order of occurrence, name the three most commonly infarcted coronary arteries.

A
  1. L anterior descending a.
  2. R coronary a.
  3. L circumflex a.
81
Q

Which portions of the heart are damaged in an infarction of the LADA?

A

The anterior wall of the left ventricle

+

the anterior portion of the interventricular septum

82
Q

Which portions of the heart are damaged in an infarction of the RCA?

A

The posterior wall of the left ventricle

+

the posterior portion of the interventricular septum

83
Q

Which portion of the heart is damaged in an infarction of the left circumflex artery?

A

The lateral wall of the left ventricle

84
Q

True/False.

Myocardial infarctions typically spare the right ventricle and atria.

A

True.

85
Q

The very initial phase of an AMI shows ST segment ____________.

The subsequent phases of an AMI shows ST segment ____________.

A

The very initial phase of an AMI shows ST segment depression.

(subendocardial)

The subsequent phases of an AMI shows ST segment elevation.

(transmural​)

86
Q

Describe the various cardiac markers used in diagnosing AMI.

A
87
Q

Troponin I is typically used in clinical diagnosis of AMI because it has early onset (___ hrs), sensitive, specific (only found in cardiac myocytes), and lasts long (___ hrs).

A

Troponin I is typically used in clinical diagnosis of AMI because it has early onset (4 hrs), sensitive, specific (only found in cardiac myocytes), and lasts long (40 hrs).

88
Q

Describe the effects of the various infarctions on myocardial tissue:

Permanent vessel occlusion

Global hypotension

Microinfarcts

A
89
Q

In myocardial infarctions, troponin I rises after _______ hours, peaks by 24 hours, and returns to normal by 7 - 10 days.

A

In myocardial infarctions, troponin I rises after 2 - 4 hours, peaks by 24 hours, and returns to normal by 7 - 10 days.

90
Q

In myocardial infarctions, troponin I rises after 2 - 4 hours, peaks by _____ hours, and returns to normal by 7 - 10 days.

A

In myocardial infarctions, troponin I rises after 2 - 4 hours, peaks by 24 hours, and returns to normal by 7 - 10 days.

91
Q

In myocardial infarctions, troponin I rises after 2 - 4 hours, peaks by 24 hours, and returns to normal by _____ days.

A

In myocardial infarctions, troponin I rises after 2 - 4 hours, peaks by 24 hours, and returns to normal by 7 - 10 days.

92
Q

In myocardial infarctions, CK-MB rises after _______ hours, peaks by 24 hours, and returns to normal by 7 - 10 days.

A

In myocardial infarctions, CK-MB rises after 4 - 6 hours, peaks by 24 hours, and returns to normal by 3 days.

93
Q

In myocardial infarctions, CK-MB rises after 4 - 6 hours, peaks by ____ hours, and returns to normal by 3 days.

A

In myocardial infarctions, CK-MB rises after 4 - 6 hours, peaks by 24 hours, and returns to normal by 3 days.

94
Q

In myocardial infarctions, CK-MB rises after 4 - 6 hours, peaks by 24 hours, and returns to normal by _____ days.

A

In myocardial infarctions, CK-MB rises after 4 - 6 hours, peaks by 24 hours, and returns to normal by 3 days.

95
Q

What is CK-MB most useful for in diagnosing AMI?

A

Diagnosing a suspected second AMI

(troponin stays in the blood stream for a week or more; CK-MB is gone after 3 days)

96
Q

What medication is given as an antiarrhythmic in patients with AMIs?

A

Beta blockers

97
Q

Why are ACE inhibitors administered in patients with AMIs?

A

To reduce cardiac remodelling

(and left ventricular dilatation)

98
Q

The Pathoma method of remembering the phases of histological change post-MI:

______ < 1 day > ______ < 1 week > ______ < 1 month > ______

A

The Pathoma method of remembering the phases of histological change post-MI:

Coagulation necrosis < 1 day > Inflammation (acute, then chronic) < 1 week > Granulation tissue < 1 month > Scarring

99
Q

What is the microscopic change in heart muscle in the first four hours after an infarction?

A

None

100
Q

What is the microscopic change in heart muscle 4 - 24 hours after an infarction?

A

Coagulative necrosis

101
Q

What is the microscopic change in heart muscle at 1 - 3 days after an infarction?

A

Neutrophilic infiltrate

102
Q

What is the microscopic change in heart muscle at 4 - 7 days after an infarction?

A

Monocyte infiltrate

103
Q

What is the microscopic change in heart muscle at 1 - 3 weeks after an infarction?

A

Granulation tissue

+

fibroblasts, collagen, and blood vessels

104
Q

What is the microscopic change in heart muscle months after an infarction?

A

Fibrosis

105
Q

Name some of the complications associated with acute myocardial infarction.

A

Arrhythmias

Left ventricular failure

Cardiogenic shock

Myocardial rupture

Thrombosis

Ventricular aneurysm

Valvular incompetence

Sudden cardiac death

106
Q

Describe the histology of infarcted myocardial tissue after 1 day.

A
107
Q

Describe the histology of infarcted myocardial tissue after 3-4 days.

A
108
Q

Describe the histology of infarcted myocardial tissue after 1 week.

A
109
Q

Describe the histology of infarcted myocardial tissue after 2-4 weeks.

A
110
Q

Describe the histology of infarcted myocardial tissue after months.

A
111
Q

What gross and microscopic features are visible during the first hour of AMI (reversible stage)?

A

None

112
Q

What gross and microscopic features are visible at ~4 hours of AMI (irreversible stage)?

A

None

113
Q

Describe the changes in gross myocardial appearance:

0 - 4 hours — None

4 - 24 hours

1 - 10 days

2 weeks

2 months — Gray-white scar

A

0 - 4 hours — None

4 - 24 hours — Dark mottling

1 - 10 days — Yellow-tan infarct and softening

2 weeks — Red-gray mottling

2 months — Gray-white scar

114
Q

Describe the changes in gross myocardial appearance:

0 - 4 hours

4 - 24 hours

1 - 10 days

2 weeksRed-gray mottling

2 monthsGray-white scar

A

0 - 4 hours — None

4 - 24 hours — Dark mottling

1 - 10 days — Yellow-tan infarct and softening

2 weeks — Red-gray mottling

2 months — Gray-white scar

115
Q

A patient is most at-risk for which complication in the first 24 hours post-MI?

A

Arrhythmia

116
Q

When is a patient most at-risk for cardiogenic shock and heart failure post-MI?

A

The first 4 hours

117
Q

When is a patient at most risk of developing fibrinous pericarditis following an MI?

A

1 - 3 days

(transmural inflammation / neutrophil infiltrate in myocardium)

118
Q

A patient is at-risk for what complications 4 - 7 days post-MI?

A

Ruptures

(ventricular free wall, interventricular septum, papillary muscle)

(macrophage phase — destroying dead tissue)

119
Q

A patient is at-risk for what complications months post-MI?

A

Aneurysm (and mural thrombus), Dressler’s syndrome

120
Q

Occlusion of which coronary artery is most likely to lead to papillary muscle rupture?

A

The RCA

121
Q

What form of cardiomyopathy is associated with HIV?

A

Systolic heart failure

(dilated cardiomyopathy)

122
Q

What form of cardiomyopathy is associated with multiple myeloma?

A

Restrictive cardiomyopathy

(amyloid deposits)

123
Q

Metastases to the heart often present as ______-sided heart failure.

A

Metastases to the heart often present as left-sided heart failure.

124
Q

Doxorubicin-induced cardiomyopathy often presents as ______-sided heart failure.

A

Doxorubicin-induced cardiomyopathy often presents as left-sided heart failure.

125
Q

What form of cardiomyopathy is associated with tuberculosis infection?

A

Constrictive cardiomyopathy

(calcified pericardium)