A 70-year-old woman comes to the office due to progressive exertional dyspnea over the last year. She has no chest pain or lower-extremity swelling. The patient has long-standing hypertension but has not always been adherent to her medical regimen. She is a lifetime nonsmoker. Blood pressure is 164/73 mm Hg and pulse is 88/min and regular. An S4 is heard on cardiac auscultation. The lungs are clear. Echocardiogram reveals left atrial enlargement, moderate concentric left ventricular hypertrophy, and a left ventricular ejection fraction of 67%. Which of the following changes are most likely to be seen in this patient?

Question

A 70-year-old woman comes to the office due to progressive exertional dyspnea over the last year.  She has no chest pain or lower-extremity swelling.  The patient has long-standing hypertension but has not always been adherent to her medical regimen.  She is a lifetime nonsmoker.  Blood pressure is 164/73 mm Hg and pulse is 88/min and regular.  An S4 is heard on cardiac auscultation.  The lungs are clear.  Echocardiogram reveals left atrial enlargement, moderate concentric left ventricular hypertrophy, and a left ventricular ejection fraction of 67%.  Which of the following changes are most likely to be seen in this patient?

Quizplus · Accepted Answer

This patient's clinical presentation and echocardiography findings are consistent with concentric left ventricular (LV) hypertrophy leading to impaired diastolic functioning (heart failure with preserved ejection fraction). In response to LV pressure overload (eg, prolonged systemic hypertension), there is upregulation of genes encoding for contractile proteins of the cardiac sarcomere, including beta-myosin heavy chain. The additional contractile fibers are added in parallel to increase the contractile strength of the LV wall. Although LV contractility and ejection fraction are increased, the thickened LV walls are now stiff and less compliant, which is often evidenced by an S4 on cardiac auscultation as blood strikes the stiff LV wall during atrial systole. Subsequent impaired diastolic filling of the noncompliant left ventricle leads to reduced stroke volume with reduced cardiac output and decreased renal perfusion. Falsely sensing a need to increase blood volume and organ perfusion, the kidneys activate the renin-angiotensin-aldosterone system (RAAS) to stimulate sodium retention (via increased aldosterone) and vasoconstriction (via increased angiotensin II). Although this response can temporarily maintain cardiac output, the increasing fluid retention will ultimately precipitate decompensated heart failure. (Choices B, C, E, and F) These combinations of changes in LV compliance, angiotensin II signaling, and beta-myosin heavy chain expression are not consistent with readily identifiable, untreated disease processes. (Choice D) Increases in LV compliance, angiotensin II signaling, and beta-myosin heavy chain expression are consistent with heart failure with reduced ejection fraction due to dilated cardiomyopathy. There is upregulation of contractile proteins; however, this occurs in response to volume overload rather than pressure overload, and therefore the contractile fibers are added in series (ie, eccentric hypertrophy) rather than in parallel. This leads to dilation of the LV cavity with increased wall compliance and decreased contractility. Reduced cardiac output with subsequent activation of the RAAS results in increased angiotensin II signaling. Educational objective: Prolonged systemic hypertension leads to concentric left ventricular (LV) hypertrophy via the addition of myocardial contractile fibers in parallel. The thickening of the LV walls reduces LV compliance, leading to impaired diastolic filling and heart failure with preserved ejection fraction. In response to reduced cardiac output, the kidneys activate the renin-angiotensin-aldosterone system, stimulating sodium retention and vasoconstriction that worsens volume overload and can lead to decompensated heart failure.

A 70-Year-Old Woman Comes to the Office Due to Progressive