3. Hypertensive heart disease (HHD)1.ppt

.

1. Hypertensive heart disease (HHD)
Causes pressure overload &
ventricular hypertrophy

2. Outline: HHD
•Hypertension
•Systemic hypertension => left sided HHD
•Pulmonary hypertension => right-sided HHD - Cor
Pulmonale

3. Hypertension
•Sustained blood pressure ≥ 140/90 mm Hg
•Newest guidelines, >120/80 constitute clinically significant
elevations in blood pressure
•Tends to rise with age, heritable, common in blacks
•95% 1
0
or idiopathic or essential hypertension)
•5% 2
0
(renal, adrenal diseases, renal artery atherosclerosis)
•Without appropriate treatment, some 50% of hypertensive
patients die of ischemic heart disease (IHD) or congestive
heart failure, and another third succumb to stroke

4. Systemic (left sided) HHD
•Pressure overload =>
ventricular hypertrophy
•Eventually hypertrophy
becomes maladaptive
•Leads to myocardial
dysfunction, myocardial
ischemia, cardiac dilation,
CHF, & in some cases
sudden death
LV hypertrophy

5. Systemic (left sided) HHD cont.
•Minimal pathologic criteria for the Dx
1.LV hypertrophy (usually concentric) in the absence of other
cardiovascular pathology e.g., aortic valve stenosis,
coarctation of the aorta &
2.A clinical history or pathologic evidence of hypertension in
other organs (e.g., kidney)
•Prolonged mild hypertension => left ventricular hypertrophy
•According to newest guidelines one-half of individuals in the
general population are hypertensive

6. Morphology: systemic HHD
•LV hypertrophy, initially
without ventricular dilation
•Heart weight > 500 g, & LV
wall thickness >2.0 cm
(normal: 1.4 cm)
•↑ LV wall thickness & ↑
interstitial connective
tissue => stiffness that
impairs diastolic filling =>
left atrial enlargement
IF
IF
Hypertrophied myocardium (>25µm)
prominent nuclear enlargement &
hyperchromasia (“boxcar nuclei”
arrows) & intercellular fibrosis (IF)

7. Clinical Features: left sided HHD
•Compensated systemic HHD may be asymptomatic (EKG or
echocardiography evidence of LV enlargement)
•Many present with atrial fibrillation (induced by left atrial
enlargement), or progressive CHF
•May develop IHD (coronary atherosclerosis & ↑ O
2 demand
from the hypertrophic muscle); renal damage or
cerebrovascular stroke; progresssive heart failure or SCD
•Control of hypertension can prevent cardiac hypertrophy &
can lead to its regression
•With normalization of BP, the associated risks of HHD are
diminished

8. Pulmonary (right-sided) HHD (Cor Pulmonale)
•Acute or chronic
•Chronic cor pulmonale
RV hypertrophy & dilation & right-sided failure, causes:
disorders of the lungs (emphysema), & 1
0
pulmonary
hypertension
RV dilation & hypertrophy caused by LV failure or by
congenital heart disease is excluded
•Acute cor pulmonale can follow massive pulmonary
embolism

9. Disorders Predisposing to Cor Pulmonale

10. Morphology: Cor Pulmonale
•In acute Cor Pulmonale
Dilation of the RV without hypertrophy
If an embolism causes sudden death, the heart may even be
of normal size
•In chronic Cor Pulmonale
Right ventricular & right atrial hypertrophy
In right ventricular failure, right ventricle & atrium dilated
Pulmonary arteries contain atheromatous plaques due to
longstanding pressure elevations

11. HHD, systemic & pulmonary
A) Systemic (left-sided) HHD. There is marked concentric thickening of the LV wall causing reduction in
lumen size. The LV & LA (asterisk) are on the right in this apical four-chamber view of the heart. A
pacemaker is present in the RV (arrow). (B) Pulmonary (right-sided) hypertensive heart disease (cor
pulmonale). The RV is markedly dilated & has a thickened free wall & hypertrophied trabeculae (apical
four-chamber view of heart, right ventricle on left). The shape of the LV (to the right) has been distorted
by the enlarged RV.
Lt. Sided
Rt. Sided