what's new in hypertensive heart disease. All forms of LVH can exist. eccentric hypertrophy can exist denovo or after MI

1. By
Dr. Agho E. John
MWACP,MBBS(AAU), BSc( Ed) Biology, ( AAU)
NCE,(Benin),

2. Overview
Definition
Epidemiology
Etiopathophysiology
Clinical features
Investigations
Diagnosis
Treatment
Prognosis
What’s new.
outline

3.  Uncontrolled and prolonged elevation of BP can
lead to a variety of changes in the myocardial
structure, coronary vasculature, and conduction
system of the heart.These changes in turn can
lead to the development of left ventricular
hypertrophy (LVH), coronary artery disease (CAD),
various conduction system diseases, and systolic
and diastolic dysfunction of the myocardium,
complications that manifest clinically as angina or
myocardial infarction, cardiac arrhythmias
(especially atrial fibrillation), and congestive heart
failure ( CHF).
OVERVIEW

4.  Hypertension remains a major public health problem associated
with considerable morbidity and mortality. Hypertensive heart
disease is a constellation of abnormalities that includes left
ventricular hypertrophy (LVH), systolic and diastolic dysfunction,
and their clinical manifestations including arrhythmias and
symptomatic heart failure.
 The classic paradigm of hypertensive heart disease is that the left
ventricular (LV) wall thickens in response to elevated blood
pressure as a compensatory mechanism to minimize wall stress.
Subsequently, after a series of poorly characterized events
(“transition to failure”), the left ventricle dilates, and the LV
ejection fraction (EF) declines (defined herein as “dilated cardiac
failure”)

5. Mark H. Drazner. Circulation. The Progression of Hypertensive Heart
Disease, Volume: 123, Issue: 3, Pages: 327-334, DOI:
(10.1161/CIRCULATIONAHA.108.845792) © 2011 American Heart Association, Inc.

6. Thus, hypertensive heart disease is a
term applied generally to heart diseases,
such as LVH , coronary artery disease,
cardiac arrhythmias, and CHF, that are
caused by the direct or indirect effects of
hypertension.
Definition

8.  The prevalence of hypertension is higher in men than in women younger
than 55 years, but the rate is higher in women older than 55 years.The
prevalence of hypertensive heart disease probably follows the same
pattern and is affected by the severity of BP increase.
 Although the exact frequency of LVH is unknown, its rate based on
electrocardiographic (ECG) findings is 2.9% for men and 1.5% for women.
The rate of LVH based on echocardiographic findings is 15-20%. Of
patients without LVH, 33% have evidence of asymptomatic LV diastolic
dysfunction.
Epidemiology

10. The prevalence in sub-Saharan Africa ranges from 12-29%. Urban figures in
Nigeria up to 40%

11. Etiology
 The etiology of hypertensive heart disease is a complex interplay of
various hemodynamic, structural, neuroendocrine, cellular, and molecular
factors.These factors play integral roles in the development of
hypertension and its complications, however, elevated blood pressure
(BP) itself can modulate these factors
 Elevated BP leads to adverse changes in cardiac structure and function in
two ways:
 1. directly, by increased afterload,
 2. indirectly, by associated neurohormonal and vascular changes
Etiopathophysioloy

12. The pathophysiologies of the various cardiac effects of hypertension differ
for example.
1. Left ventricular hypertrophy
 Of patients with hypertension, 15-20% develop LVH.
 LVH, defined as an increase in the mass of the left ventricle, is caused by
the response of myocytes to various stimuli accompanying elevated BP.
Myocyte hypertrophy can occur as a compensatory response to increased
afterload. Mechanical and neurohormonal stimuli accompanying
hypertension can lead to activation of myocardial cell growth and gene
expression which results in LVH.
 In addition, activation of the renin-angiotensin system, through the
action of angiotensin II on angiotensin I receptors, leads to growth of
interstitium and cell matrix components.

14. Types of LVH
 Concentric LVH, and eccentric LVH. Concentric LVH is an increase in LV
thickness and LV mass with increased LV diastolic pressure and volume,
commonly observed in persons with hypertensive Heart DX
 Although the development of LVH initially plays a protective role in
response to increased wall stress to maintain adequate cardiac output, it
later leads to the development of diastolic and, ultimately, systolic
myocardial dysfunction.

16. Coronary Artery Risk Development inYoung
Adults study, although LVH was associated
with incident heart failure 15 years later
(>80% of which occurred with dilated
cardiomyopathy or LVEF <50%), the
predisposing LVH was in an eccentric and
not concentric pattern.

17. Table 1. Factors Influencing LV Geometry in
Hypertensive Patients
Pressure load: severity, duration, rapidity of
onset
Volume load
Demographic factors: age, race/ethnicity,
gender
Concomitant medical conditions: coronary
artery disease, diabetes mellitus, obesity,
valvular heart disease
Neurohormonal milieu
Alterations of the extracellular matrix
Genetic factors
Demographic factors can als

18. Left atrial abnormalities
 Frequently underappreciated, structural and functional changes of the
left atrium are very common in patients with hypertension.The increased
afterload imposed on the left atrium (LA) by the elevated LV end-diastolic
pressure secondary to increased BP leads to impairment of the left atrium
and LA appendage function, plus increased LA size and thickness.
 Increased LA size accompanying hypertension in the absence of valvular
heart disease or systolic dysfunction usually implies chronicity of
hypertension and may correlate with the severity of LV diastolic
dysfunction.
 In addition to LA structural changes, these patients are predisposed to
atrial fibrillation.

19.  Valvular disease.
1. Chronic and severe hypertension can cause aortic root dilatation, leading
to significant aortic insufficiency. Some degree of hemodynamically
insignificant aortic insufficiency is often found in patients with uncontrolled
hypertension.
2. Hypertension is also thought to accelerate the process of aortic sclerosis
and cause mitral regurgitation.

20.  Myocardial ischaemia
The development of ischemia in patients with hypertension is
multifactorial.
1. Increased afterload secondary to hypertension leads to an increase in LV
wall tension and transmural pressure, compromising coronary blood flow
during diastole.
2. the microvasculature beyond the epicardial coronary arteries has been
shown to be dysfunctional in patients with hypertension, and it may be
unable to compensate for increased metabolic and oxygen demand.
3. The development and progression of arteriosclerosis, the hallmark of
coronary artery disease, is exacerbated in arteries subjected to
chronically elevated BP.

21.  Cardiac arrhythmias
Cardiac arrhythmias commonly observed in patients with hypertension
include atrial fibrillation, premature ventricular contractions (PVCs), and
ventricular tachycardia (VT).The risk of sudden cardiac death is increased.
Various mechanisms thought to play a part in the pathogenesis of
arrhythmias;
1. altered cellular structure and metabolism, inhomogeneity of the
myocardium, poor perfusion, myocardial fibrosis, and fluctuation in
afterload
2. In one study, nearly 50% of patients with atrial fibrillation had
hypertension. Although the exact etiology is not known, LA structural
abnormalities, associated coronary artery disease, and LVH have been
suggested as possible contributing factors.

22.  Symptoms of hypertensive heart disease depend on the duration,
severity, and type of disease. In addition, the patient may or may not be
aware of the presence of hypertension.
 Left ventricular hypertrophy
Patients with left ventricular hypertrophy (LVH) alone are totally
asymptomatic, unless the LVH leads to the development of diastolic
dysfunction and heart failure
 Myocardial ischemia
A heaviness, pressure, and/or squeezing
Radiating to the neck, jaw, upper back, or left arm
Provoked by emotional or physical exertion
Relieved with rest or sublingual nitroglycerin
Clinical features

23.  Cardiac arrhythmias
Irregular or abnormal heart rhythms can cause a variety of symptoms,
including the following:
Palpitations
Near or total syncope
Precipitation of angina
Sudden cardiac death
Precipitation of heart failure, especially with atrial fibrillation in diastolic
dysfunction

24. Physical Examination
Physical signs of hypertensive heart disease depend on the predominant
cardiac abnormality and the duration and severity of the hypertensive heart
disease. Findings from the physical examination may be entirely normal in
the very early stages of the disease, or the patient may have classic signs
upon examination.

25. Pulses
The arterial pulses are normal in the early stages of hypertensive heart
disease.The cardiac rhythm is regular if the patient is in sinus rhythm; it is
irregularly irregular if the patient is in atrial fibrillation.The heart rate is as
follows:
Normal in patients in sinus rhythm
Not normal in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial
fibrillation and a rapid ventricular response
The pulse volume is usually normal, but it is decreased in patients with left
ventricular (LV) dysfunction. Additional findings may include radial-femoral
delay if the etiology of hypertension is coarctation of the aorta

26. Heart
 A presystolic S4 may be felt. Later in the course of disease, when significant
systolic LV dysfunction supervenes, the apical impulse is displaced laterally,
owing to LV dilatation. In the right ventricle, a lift is present late in the course
of heart failure if significant pulmonary hypertension develops.
 S2 at the right upper sternal border is loud because of an accentuated aortic
component (A2).
 It can have a reverse or paradoxical split due either to increased afterload or
to associated left bundle-branch block (LBBB).
 S4 is frequently palpable and audible, implying the presence of a stiffened,
noncompliant ventricle due to chronic pressure overload and LV hypertrophy
(LVH).
 S3 is not typically present initially, but it is audible in the presence of heart
failure.
 A holosystolic murmur of mitral regurgitation may be present in patients with
advanced heart failure and a dilated mitral annulus.

27.  The tests to be ordered depend on clinical judgment regarding the
etiology of hypertension.
Electrocardiogram
Urinalysis
Blood glucose and hematocrit levels
Serum potassium, creatinine (or the corresponding estimated glomerular
filtration rate [GFR]), and calcium measurements
Lipid profile after a 9- to 12-hour fast - Includes high density lipoprotein
(HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and
triglycerides
 TFT
Investigation/ diagnosis

28. Transthoracic Echocardiography
Transthoracic echocardiography (TTE) may be very useful for identifying
features of hypertensive heart disease. [20]TTE is more sensitive and specific
then electrocardiography for diagnosing the presence of left ventricular (LV)
hypertrophy (LVH) (57% for mild and 98% for severe LVH). LVH is
symmetrical, whereas the hypertrophy of hypertrophic cardiomyopathy is
asymmetrical.
 Systolic dysfunction
Evidence of LV systolic dysfunction includes a dilated LV, low LV fractional
shortening, low LV ejection fraction, and the presence of systolic
dysfunction, which is commonly associated with some degree of diastolic
dysfunction.

29.  Chest radiographs may show notching of the undersurface of the ribs
from the development of collateral circulation in coarctation of the aorta;
cardiomegaly in late stages of the disease, due to LV dilatation;
cephalization of pulmonary blood flow, Kerley B lines, and alveolar
infiltrates in the presence of elevated left ventricular (LV) end-diastolic
pressure and pulmonary congestion; and blunting of the costophrenic
angle in the presence of pleural effusion.
Electrocardiography
A 12-lead electrocardiogram (ECG) may show a variety of abnormalities. For
example, ischemic ECG changes may be found in individuals presenting with
hypertensive crisis in whom no significant coronary atherosclerosis is
detectable by coronary angiography. Evidence of left atrial (LA) enlargement
includes broad P waves in the limb leads and a prominent and wide others
are LVH criteria, Bundle branch blocks and arrythmias

30. PRINCIPLES OF MANAGEMENT OF HHDX
•CONTROL BP
•REGRESSION OF LVH-RAAS (arb>acei)>CCB>DIUR(mra>thiaz)>BB
•PREVENTION OF PROGRESSION -STATINS
Treatment

31. The treatment of hypertension and hypertensive heart disease can involve
the following classes of antihypertensive medications:
Thiazide diuretics
Beta blockers and combined alpha and beta blockers
Calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin-receptor blockers (ARBs)
Direct vasodilators (eg, hydralazine)
Angiotensin receptor neprilysin inhibitor (ARNI) for systolic heart failure

32. ACE inhibitors and ARBs
ACE inhibitors are the first choice in patients with diabetes and/or
ventricular dysfunction. ARBs are a reasonable alternative, especially for
patients who suffer adverse effects from ACE inhibitors.
Beta blockers
Beta blockers are the drugs of first choice in patients with heart failure due
to systolic left ventricular (LV) dysfunction, patients with ischemic heart
disease with or without a history of myocardial infarction, and patients with
thyrotoxicosis.

33. Treatment of left ventricular systolic dysfunction
 Diuretics (predominantly loop diuretics) are used in the treatment of LV
systolic dysfunction. Low-dose spironolactone has been shown to
decrease the rates of morbidity and mortality in patients in NYHA class III
or IV heart failure who are already taking ACE inhibitors.This agent is also
recommended for use in post-myocardial infarction patients with
diabetes mellitus or who have an LV ejection fraction of less than 40%.
 The angiotensin receptor neprilysin inhibitor (ARNI) sacubitril/valsartan
has been shown to be superior to ACE inhibitor alone in reducing the risk
of death and hospitalization in patients with heart failure due to systolic
dysfunction and is now preferred over ACE Inhibitots and ARBs.

34. Treatment of cardiac arrhythmias
The treatment of these conditions depends upon the specific arrhythmia and
the underlying LV function, Anticoagulation should be considered in patients
with atrial fibrillation. In addition, treat anxiety, stress, sleep apnea, and
other contributing or precipitating factors.

35. Mortality and morbidity rates from hypertensive heart disease are higher
than those of the general population and depend on the specific cardiac
pathology.Data suggest that increases in mortality and morbidity rates are
related more to the pulse pressure than to the absolute systolic or diastolic
blood pressure (BP) levels, but all are important.
1. The development of left ventricular (LV) hypertrophy (LVH) is clearly
related to an increase in the cardiovascular mortality rate.
2. Left ventricular diastolic dysfunction
The prognosis of patients with diastolic dysfunction is poor and is affected
by the presence of underlying coronary artery disease, Even in patients with
asymptomatic diastolic dysfunction due to hypertension, the risk of all-
cause mortality and cardiovascular events is significantly increased.
Prognosis

36. What’s new.

37. Challenges to the Classic Paradigm of the Progression of
Hypertensive Heart Disease
In animal models of pressure overload, concentric LVH can be blocked and
dilated cardiac failure does not develop.
In humans, concentric LVH does not commonly progress to dilated cardiac
failure in the absence of myocardial infarction.
Some hypertensive subjects develop dilated cardiac failure without
antecedent concentric LVH and without clinical evidence of myocardial
infarction.

38. Hypertensive heart disease encompasses a broad spectrum including
asymptomatic LVH and clinical heart failure however, there is considerable
interindividual variability in the progression from hypertension to LVH in
both the magnitude of the increase in LV mass and its geometric pattern.
In conclusion

39. THANKYOU.

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