In the clinical setting, physicians typically discriminate between left-sided heart failure and right-sided heart failure. Left-sided heart failure is further classified as either systolic heart failure, where the left ventricle fails to contract normally and, as a result, cannot push/eject enough blood into the circulation or diastolic failure where the ventricle becomes stiff and cannot adequately fill with blood between cardiac cycles. This reduced capacity from normal to (partly) reduced left ventricular ejection fraction (LVEF) can be categorized into heart failure with preserved ejection fraction (HFpEF, LVEF >50%), heart failure with mid-range ejection fraction (HFmrEF, LVEF 40% to 49%), and heart failure with reduced ejection fraction (HFrEF, LVEF <40% from normal)1. Left-sided heart failure affects the transportation of oxygen-rich blood from the lungs to the rest of the body, causing retention of blood, and therefore congestion in the lungs. This congestion affects breathing and thus causes increased fatigue and reduced oxygenation in the blood. Other clinical manifestations of heart failure include enlargement of the heart, due to compensation by the left ventricle.
Right-sided failure (pulmonary circulation) is usually, but not always, resultant from left-sided failure. In such cases, right-sided heart failure often results from pulmonary heart diseases like pulmonary hypertension and pulmonary artery stenosis. Physical observations include peripheral edema, ascites, and liver enlargement, while increased pressure in the jugular vein will be present as a marker of fluid retention. Right-sided heart failure thus leads to congested systemic capillaries generating excess fluid accumulation in the body (edema) as well as potential Nocturia (frequent nighttime urination). In increasingly severe cases, ascites and liver enlargement may develop with subsequent complications.
Preliminary diagnosis of heart failure is achieved by considering patient history and performing a physical examination. The main symptoms presented during examination include dyspnea and fatigue, intolerance to exercise, and peripheral and/or pulmonary edema. Conclusive diagnosis in the clinical setting for heart failure patients is to run a 2-dimensional echocardiogram scan coupled with Doppler flow studies.
Treatment/interventions which have had some success with heart failure patients include cardiac resynchronization therapy and implantable cardioverter-defibrillators, angiotensin receptor blockers, beta-blockers, ACE inhibitors, hydralazine and nitrates, or aldosterone antagonists. In the most severe cases, patients have undergone cardiac transplant surgery if they were eligible.
With all the progress made in the field, researchers continue to investigate the underlying causes and mechanisms of heart failure and explore safer and more effective strategies to treat and manage the disease. Scientists have developed numerous research models that have become prevalent in cardiovascular research labs and this article will focus on one particular model that has significantly enhanced the ability for scientific discovery. The transverse aortic constriction model (or TAC banding model) results in left-sided heart failure through pressure overload partial occlusion of the transverse aorta. This procedure often leads to cardiac hypertrophy, a common compensatory mechanism in heart failure and, in some animals, will result in heart failure over time. Disease progression in this model, and ultimately the development of heart failure, depends on several factors as will be discussed below. Thus, having a means to non-invasively confirm surgical success, monitor progression, and confirm heart failure is key to ongoing research efforts to find new therapeutic targets.