Valentine’s day can be a happy, candy-and-flowers day – but it can also be a day of loneliness and melancholy. Today’s post, written by our medical student correspondent Richard Huang, addresses the darker side of this Day of the Heart. 

While it is impossible to die directly from heartbreak (although those going through it sure feel like they are dying), it is quite possible to die from a broken heart, i.e. heart failure.

One of the main causes of heart failure is dilated cardiomyopathy. Dilated cardiomyopathy is a chronic and progressive disease with many causes, the most common being complications from the Big Three: coronary artery disease, hypertension, and diabetes. In this post, we will systematically examine dilated cardiomyopathy by going from the small to the big, starting with microscopic morphology and then moving up to gross changes. From there, we will see how the pathology correlates with the disease’s pathophysiology, and how the pathophysiology produces the clinical signs and symptoms.

The basic mechanism underlying dilated cardiomyopathy is as follows:

  1. Increase in preload of the heart increases the pressure in the ventricles.
  2. Sustained increase in pressure in the ventricles increases the stress on the ventricular walls.
  3. Increased wall stress modifies ventricular cardiomyocytes’ gene expression.
  4. Gene expression changes result in the duplication of sarcomeres to accommodate the increase in preload.

In order to accommodate the increase in preload, the sarcomeres duplicate in series to increase the ventricular volume, causing individual cardiomyocytes to increase in length. This microscopic change is reflected anatomically by large, dilated heart chambers with relatively normal wall thickness (since the sarcomeres do not duplicate much in parallel, which would have thickened the heart walls).


Massively dilated heart in a case of dilated cardiomyopathy

Physiologically, the increased preload increases the cardiac output of the heart by the Frank-Starling mechanism: increased preload stretches the heart, leading to increased cross-bridging between actin and myosin filaments, resulting in increased active tension in cardiomyocytes (thereby increasing the contractile force necessary to eject the increased preload).

However, as the heart continues to dilate to compensate for the increased preload, it becomes overstretched and falls off the length-tension curve (below). That is, when the heart is overstretched, the number of cross-bridges between actin and myosin filaments actually decreases, and the active tension in cardiomyocytes drops. This leads to reduced contractile force of the heart, and the inevitable systolic heart failure. And we all know what happens once the heart fails.


The clinical presentation of dilated cardiomyopathy is essentially dictated by the resultant heart failure. The physical exam reveals signs and symptoms consistent with progressive heart failure, which typically include:

  • Tachycardia: heart failure reduces perfusion, which triggers baroreceptors to increase the heart rate in order to maintain cardiac output
  • Tachypnea: heart failure reduces perfusion, causing hypoxia, which increases PCO2 and decreases PO2, leading to a compensatory increase in respiratory rate
  • Hypertension: heart failure reduces perfusion, which stimulates neurohormonal compensatory mechanisms, leading to release of catecholamines by the adrenergic nervous system and the activation of the renin-angiotensin-aldosterone system. Both lead to increased peripheral vascular resistance, and subsequently increased blood pressure.
  • Jugular venous distension: heart failure backs up blood into the venous vasculature, which distends neck veins.
  • Lung crackles: heart failure backs up blood into the pulmonary vasculature, which increases hydrostatic pressure, which pushes fluid out of the capillary into the interstitium (resulting in pulmonary edema). The increased interstitial pressure collapses distal airways, and on inspiration, airways snap open, producing crackling sounds on auscultation.
  • Peripheral edema: heart failure backs up blood into the peripheral venous vasculature, which increases hydrostatic pressure, pushing fluid out of vasculature into the interstitium. The accumulation of fluid in peripheral tissues causes tissue swelling (edema).
  • Heart murmurs: inflow of blood from the atrium into a fluid-overloaded ventricle sloshes the blood against the ventricle walls. The reverberation produces a diastolic heart sound (the S3 gallop). (Note: Progressive dilation of the heart can lead to the development of mitral and tricuspid regurgitation, which would present as additional heart murmurs.)
  • Displaced point of maximal impulse: the dilated heart shifts the point of maximal impulse away from its usual location.
  • Cyanosis: heart failure reduces perfusion, which causes hypoxia, increasing the concentration of deoxygenated hemoglobin (which is blue in color).