A 55-year-old man comes to the office for follow-up. The patient was diagnosed with hypertension 3 weeks ago, and an ECG performed at that time showed features of left ventricular hypertrophy. He was subsequently referred for echocardiography. The patient feels well and has had no shortness of breath, fatigue, or leg swelling. He has no other medical conditions, takes no medications, and does not use tobacco, alcohol, or illicit drugs. Blood pressure is 155/90 mm Hg and pulse is 80/min. BMI is 35 kg/m². Physical examination shows normal jugular venous pressure. There are no lung crackles, heart gallops, or lower extremity edema. Echocardiography reveals a left ventricular ejection fraction of 30%. Which of the following patterns of chemical mediators is most likely present in this patient?

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11ec160b_3a74_62cf_9249_3fa5a6cc99c2_MD0001_00 This patient's echocardiography reveals a reduced left ventricular (LV) ejection fraction (<50%) in the absence of heart failure symptoms, a condition known as asymptomatic left ventricular systolic dysfunction. An early asymptomatic period is common in the progression of heart failure; it occurs in part due to compensatory eccentric hypertrophy in response to LV volume overload. In addition, neurohormonal mechanisms help maintain cardiac output and organ perfusion in the setting of declining cardiac function. Early in the course of heart failure, small reductions in cardiac output lead to decreased stretch of aortic and carotid baroreceptors with consequent sympathetic nervous system activation (increased norepinephrine) to stimulate vasoconstriction, increased heart rate, and increased cardiac contractility. In addition, decreased renal perfusion stimulates the juxtaglomerular apparatus to increase renin secretion and activate the renin-angiotensin-aldosterone system (RAAS), leading to vasoconstriction via increased angiotensin II levels and salt and water retention via increased aldosterone levels. The volume retention (increased preload) and vasoconstriction (increased afterload) help maintain cardiac output and organ perfusion in the short term; however, the long-term effects are deleterious because increased hemodynamic stress and neurohormonal-induced cardiac remodeling eventually lead to decompensated heart failure. Atrial and ventricular myocardial stretch triggers increased atrial and brain natriuretic peptide secretion through separate neurohormonal pathways. These peptides stimulate vasodilation and salt and water excretion, counteracting the effects of the sympathetic nervous system and RAAS; however, the natriuretic pathways are eventually overwhelmed by the downward compensatory spiral. Educational objective: Asymptomatic left ventricular systolic dysfunction is a common stage in the progression of heart failure. Neurohormonal mechanisms, including the sympathetic nervous system and renin-angiotensin-aldosterone system, help maintain the asymptomatic period by increasing volume retention and peripheral resistance to maintain organ perfusion. Although these mechanisms are beneficial in the short term, they are ultimately deleterious, increasing hemodynamic stress and cardiac remodeling that eventually lead to decompensated heart failure.

A 55-Year-Old Man Comes to the Office for Follow-Up