The document discusses myocardial infarction (MI), detailing reperfusion methods, contributing factors to reperfusion injury, clinical features, electrocardiographic abnormalities, and laboratory evaluations that help diagnose MI. It outlines complications and consequences, including mortality rates and the impact of chronic ischemic and hypertensive heart disease, as well as characteristics of left-sided hypertensive heart disease and cor pulmonale. Finally, it describes the morphology and clinical features associated with these conditions, emphasizing the effects of hypertension on the heart.

1. Cardiovascula
r system
Dr. Raya D. Marji, M.D
Al-Balqa Applied University
Faculty of Medicine

2. Infarct Modification by Reperfusion:
• Reperfusion is achieved by thrombolysis, angioplasty, or coronary arterial
bypass graft.
• Late restoration of blood flow can incite greater local damage: so-called
“reperfusion injury”.

3. Factors that contribute to reperfusion injury:
1. Mitochondrial dysfunction: Ischemia causes swelling and rupture of the outer
membrane, releasing mitochondrial contents>> promote apoptosis.
2. Myocyte hypercontractility: intracellular levels of calcium are increased.
Uncontrolled contraction>> cytoskeletal damage and cell death.
3. Free radicals, including superoxide anion (• − O2 ), hydrogen
peroxide (H2O2), hypochlorous acid (HOCl), nitric oxide–derived peroxynitrite,
and hydroxyl radicals (•OH).
4. Leukocyte aggregation: occlude the microvasculature and contribute to the “no-
reflow” phenomenon>> elaborate proteases and elastases.
5. Platelet and complement activation also contribute to microvascular injury.

4. Microscopy:
• Contraction band necrosis
(hypercontracted sarcomeres are created
by an influx of calcium across
plasma membranes that heightens actin-
myosin interactions)
• In the absence of ATP, the sarcomeres
cannot relax and get stuck in a tetanic
state.

6. Clinical Features:
• Severe, crushing substernal chest pain (or pressure) that can radiate
to the neck, jaw, epigastrium, or left arm.
• Pain typically lasts several minutes to hours.
• Not relieved by nitroglycerin or rest.
• Atypical signs (10% to 15%) or asymptomatic “silent” infarcts:
common in patients with underlying diabetes mellitus and in older
adults.

7. • Rapid and weak pulse, diaphoretic (sweating) and nauseous patients.
• Dyspnea is common
• Massive MIs (involving more than 40% of the left
ventricle): cardiogenic shock develops.

8. Electrocardiographic
abnormalities:
• Q waves, ST segment changes,
and T wave inversions.
• Arrhythmias.

9. The laboratory evaluation:
• Based on measuring blood levels of macromolecules that leak out of
injured myocardial cells through damaged cell membranes.
• These molecules include myoglobin, cardiac troponins T and I (TnT,
TnI), creatine kinase (CK; specifically the myocardial isoform, CK-MB),
and lactate dehydrogenase.
• Troponins (and to a lesser extent CK-MB) have high specificity and
sensitivity for myocardial damage.

11. CK-MB:
 Total CK activity is not a reliable marker of cardiac injury since
various isoforms of CK are found in non-cardiac tissues.
 CK-MB isoform—principally derived from myocardium, but also
present at low levels in skeletal muscle—is a more specific indicator of
heart damage.
 CK-MB activity begins to rise within 2 to 4 hours of MI, peaks at 24
to 48 hours, and returns to normal within approximately 72 hours.

12. Troponins:
TnI and TnT normally are not found in the circulation.
Detectable within 2 to 4 hours, with levels peaking at 48 hours
and remaining elevated for 7 to 10 days.
Persistence of elevated troponin levels allows the diagnosis of an acute MI
to be made long after CK-MB levels have returned to normal.
With reperfusion, both troponin and CK-MB levels may peak earlier owing
to more rapid washout of the enzyme from the necrotic tissue.

13. Consequences and Complications of
Myocardial Infarction
• The overall in-hospital death rate for MI is approximately 7% to 8%.
• MI associated with ST segment elevations experiencing higher
mortality rates than those without.
• Out-of-hospital mortality is poorer: one third of individuals with
STEMIs die, usually of an arrhythmia within 1 hour of symptom onset.

14. Complications of
Myocardial
Infarction:
Contractile
dysfunction
Papillary
muscle
dysfunction
Right
ventricular
infarction
Myocardial
rupture
Arrhythmias Pericarditis
Chamber
dilation
Mural
thrombus
Ventricular
aneurysm
Progressive
heart failure

16. • The risk for complications and the overall prognosis depends on
infarct size, site, and type.
• Large transmural infarcts: Cardiogenic shock, arrhythmias, and late
CHF.
• Anterior transmural MIs: Free wall rupture, expansion, aneurysm
formation, and formation of mural thrombi.
• Posterior transmural infarcts: conduction blocks, right ventricular
involvement, or both.
• Anterior infarcts have a much more guarded prognosis than those
with posterior infarcts.

17. Ventricular remodeling
• Noninfarcted regions undergo hypertrophy and dilation, in
combination with the scarring and thinning of the infarcted zones.
• The overall mortality rate within the first year is about 30%, including
deaths occurring before the patient reaches the hospital.
• The annual mortality rate for patients who have suffered an MI is 3%
to 4%.

18. Chronic Ischemic Heart Disease
• Ischemic cardiomyopathy.
• Progressive heart failure secondary to ischemic myocardial damage.
• Chronic IHD appears when the compensatory mechanisms (e.g.,
hypertrophy) of residual myocardium begin to fail.
• Severe CAD can cause diffuse myocardial dysfunction, and even
micro-infarction and replacement fibrosis, without any clinically
evident episode of frank infarction.
• The heart failure of chronic IHD is typically severe and is occasionally
has new episodes of angina or infarction.

19. HYPERTENSIVE HEART DISEASE
• A consequence of the increased demands placed on the heart by
hypertension.
• Causes pressure overload and ventricular hypertrophy.
• Myocyte hypertrophy is an adaptive response to pressure overload;
persistent hypertension eventually can culminate in dysfunction,
cardiac dilation, CHF, and even sudden death.

20. Hypertensive Heart disease:
• Left-sided hypertensive changes,
secondary to systemic
hypertension.
• Right-sided
hypertensive changes—so-called
“cor pulmonale.”
• Pulmonary hypertension.

21. Systemic (Left-Sided) Hypertensive Heart
Disease
• The criteria for the diagnosis of systemic hypertensive heart disease:
(1) Left ventricular hypertrophy in the absence of other cardiovascular
pathology (e.g., valvular stenosis).
(2) History or pathologic evidence of hypertension.

22. MORPHOLOGY
• Left ventricular hypertrophy, typically without ventricular dilation until very late in
the process.
• The heart weight can exceed 500 g (normal for a 60- to 70-kg individual is 320 to 360
g), and the left ventricular wall thickness can exceed 2.0 cm (normal is 1.2 to 1.4 cm).
• Left ventricular wall thickness imparts a stiffness that impairs diastolic filling and can
result in left atrial dilation.
• In long-standing systemic hypertensive heart disease leading to congestive failure,
the hypertrophic left ventricle typically is dilated.
• Microscopically, the transverse diameter of myocytes is increased and there is
prominent nuclear enlargement and hyperchromasia (“boxcar nuclei”), as well as
intercellular fibrosis.

23. • In long-standing systemic
hypertensive heart disease leading
to congestive failure, the
hypertrophic left ventricle typically is
dilated.
• Microscopically, the transverse
diameter of myocytes is increased
and there is prominent nuclear
enlargement
and hyperchromasia (“boxcar nuclei
”), as well as intercellular fibrosis.

24. Systemic (left-sided)
hypertensive heart
disease
• Concentric thickening of the left
ventricular wall causing reduction in
lumen size.
• Left atrial dilation (asterisk) due to
stiffening of the left ventricle and
impaired diastolic relaxation, leading
to atrial volume overload.

25. Left ventricular hypertrophy

26. Clinical Features
• Compensated HHD: asymptomatic or:
1- Elevated blood pressure on routine physical examination.
2- ECG or echocardiographic findings of left ventricular hypertrophy.
3- Onset of atrial fibrillation (secondary to left atrial enlargement)
and/or CHF.

27. Prognosis:
• Depending on the severity and duration of the condition, the
underlying cause of hypertension, and the adequacy of therapeutic
control, patients can:
(1) Enjoy normal longevity and die of unrelated causes.
(2) Develop IHD.
(3) Suffer renal damage or cerebrovascular stroke.
(4) Experience congestive heart failure.

28. Pulmonary Hypertensive Heart Disease— Cor
Pulmonale
• Right ventricular hypertrophy and dilation—frequently accompanied
by right-sided heart failure—caused by pulmonary hypertension
attributable to primary disorders of the lung parenchyma or
pulmonary vasculature.
• Right ventricular dilation and hypertrophy caused by left ventricular
failure (or by congenital heart disease) is substantially more common
but is excluded by this definition.
• Cor pulmonale can be acute in onset or can have a slow and insidious
onset.

30. MORPHOLOGY
• In acute cor pulmonale: right ventricular dilation.
** if an embolism causes sudden death, the heart may even be of
normal size.
• Chronic cor pulmonale: right ventricular (and often right atrial)
hypertrophy.
** In extreme cases, the thickness of the right ventricular wall may be
comparable to or even exceed that of the left ventricle.

31. Chronic cor pulmonale:
• The right ventricle is markedly
dilated and hypertrophied.
• Thickened free wall and
hypertrophied trabeculae.
• The shape and volume of the left
ventricle have been distorted by
the enlarged right ventricle.