A patient with long-standing hypertension has an echocardiogram showing markedly thickened LV walls and an ejection fraction of 62% (normal). She reports shortness of breath when climbing stairs. What is the most likely explanation for her symptoms?
AHer ejection fraction measurement is inaccurate — systolic dysfunction must be present to explain dyspnea
BThe hypertrophied, fibrotic myocardium is stiffer than normal, impairing diastolic relaxation and requiring elevated filling pressures that back up into the pulmonary vasculature
LVH causes diastolic dysfunction even while systolic function (ejection fraction) is preserved. Interstitial fibrosis makes the myocardium stiffer; during diastole, the stiff wall resists relaxation and requires elevated filling pressures to achieve adequate end-diastolic volume. These elevated pressures transmit backward through the left atrium into the pulmonary veins, causing fluid to leak into the lungs — producing dyspnea on exertion and eventually pulmonary edema. This is the pathophysiology of 'heart failure with preserved ejection fraction' (HFpEF).
Question 2 Multiple Choice
According to the law of Laplace (wall stress = pressure × radius / 2 × wall thickness), what is the primary mechanical purpose of concentric LVH in response to chronic pressure overload?
ATo generate more total contractile force by increasing the number of sarcomere units available
BTo reduce heart rate, giving the ventricle more time to fill between beats
CTo normalize wall stress by increasing wall thickness in proportion to the elevated pressure, so each unit of wall bears the same load as before
DTo reduce ventricular chamber radius, decreasing the volume the ventricle must handle per beat
The law of Laplace shows that wall stress rises with pressure and falls with increasing wall thickness. When chronic hypertension raises intracavitary pressure, the ventricle responds by adding sarcomere units in parallel (increasing fiber diameter and wall thickness), which restores wall stress toward normal values. This is an adaptive, compensatory response — but it comes at the cost of myocardial stiffness and diastolic dysfunction.
Question 3 True / False
Left ventricular hypertrophy is synonymous with heart failure — patients with LVH will have reduced ejection fractions.
TTrue
FFalse
Answer: False
LVH and heart failure are not synonymous. Many patients with severe LVH have completely normal systolic function (normal ejection fraction) and may be minimally symptomatic for years. The danger is that LVH progresses along a continuum: diastolic dysfunction appears first (stiff ventricle, elevated filling pressures), and only later — if the hypertrophic response fails and eccentric remodeling sets in — does systolic function decline and ejection fraction fall. Equating LVH with heart failure is one of the most important misconceptions to correct.
Question 4 True / False
After successful antihypertensive treatment causes regression of left ventricular wall thickness, diastolic function typically recovers at the same rate as myocyte mass recedes.
TTrue
FFalse
Answer: False
Myocyte hypertrophy (increased cell size) can reverse over months to years with effective blood pressure control. However, the interstitial fibrosis (collagen deposition) that underlies diastolic dysfunction does not reverse as readily or quickly. Because diastolic impairment is driven substantially by fibrosis rather than just myocyte mass, patients may have regression of LVH on echocardiography well before their diastolic function normalizes — and in some cases the fibrosis is partially irreversible.
Question 5 Short Answer
Explain why a patient with severe left ventricular hypertrophy and a normal ejection fraction can still develop pulmonary edema. Trace the pathophysiological mechanism step by step.
Think about your answer, then reveal below.
Model answer: LVH causes interstitial fibrosis that stiffens the myocardium. During diastole, the stiff LV resists passive relaxation, so higher filling pressures are required to stretch the wall and achieve adequate end-diastolic volume. These elevated LV filling pressures are transmitted backward to the left atrium (causing LA dilation) and then into the pulmonary veins and capillaries. When pulmonary capillary hydrostatic pressure exceeds oncotic pressure, fluid leaks into the alveolar spaces — producing pulmonary edema and dyspnea — even though the ejection fraction (systolic function) remains normal.
This mechanism is the pathophysiological basis of heart failure with preserved ejection fraction (HFpEF), and it illustrates why ejection fraction alone is insufficient to assess cardiac health. The LV can be contracting normally on every beat while still causing pulmonary congestion if it is too stiff to relax and fill properly.