Ventricular remodeling

Ventricular remodeling (or cardiac remodeling)^[1] refers to the changes in size, shape, structure and physiology of the heart. This can happen as a result of exercise (physiological remodelling) or after injury to the heart muscle (pathological remodelling).^[2] The injury is typically due to acute myocardial infarction (usually transmural or ST segment elevation infarction), but may be from a number of causes that result in increased pressure or volume overload (forms of strain) on the heart. Chronic hypertension, congenital heart disease with intracardiac shunting, and valvular heart disease may also lead to remodeling. After the insult occurs, a series of histopathological and structural changes occur in the left ventricular myocardium that lead to progressive decline in left ventricular performance. Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume.

Physiological remodelling is reversible while pathological remodelling is mostly irreversible. Remodeling of the ventricles under left/right pressure demand make mismatches inevitable. Pathologic pressure mismatches between the pulmonary and systemic circulation guide compensatory remodeling of the left and right ventricles. The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function following a remote injury or pathological process.

Concentric hypertrophy is due to pressure overload, while eccentric hypertrophy is due to volume overload.^[3]

Pathophysiology

Myocardiocyte

The cardiac myocyte is the major cell involved in remodeling. Fibroblasts, collagen, the interstitium, and the coronary vessels to a lesser extent, also play a role. A common scenario for remodeling is after myocardial infarction. There is myocardial necrosis (cell death) and disproportionate thinning of the heart. This thin, weakened area is unable to withstand the pressure and volume load on the heart in the same manner as the other healthy tissue. As a result, there is dilatation of the chamber arising from the infarct region. The initial remodeling phase after a myocardial infarction results in repair of the necrotic area and myocardial scarring that may, to some extent, be considered beneficial since there is an improvement in or maintenance of LV function and cardiac output. Over time, however, as the heart undergoes ongoing remodeling, it becomes less elliptical and more spherical. Ventricular mass and volume increase, which together adversely affect cardiac function. Eventually, diastolic function, or the heart's ability to relax between contractions may become impaired, further causing decline.

Treatment

Many factors influence the time course and extent of remodeling, including the severity of the injury, secondary events (recurrent ischemia or infarction), neurohormonal activation, genetic factors and gene expression, and treatment. Medications may attenuate remodeling. Angiotensin-converting enzyme (ACE) inhibitors have been consistently shown to decrease remodeling in animal models or transmural infarction and chronic pressure overload. Clinical trials have shown that ACE inhibitor therapy after myocardial infarction leads to improved myocardial performance, improved ejection fraction, and decreased mortality compared to patients treated with placebo. Likewise, inhibition of aldosterone, either directly or indirectly, leads to improvement in remodeling.^[4] Carvedilol,a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function.^[5] Early correction of congenital heart defects, if appropriate, may prevent remodeling, as will treatment of chronic hypertension or valvular heart disease. Often, reverse remodeling, or improvement in left ventricular function, will also be seen.

See also

• Dor procedure

References

Further reading

• "Left Ventricular Remodeling in Heart Failure: Current Concepts in Clinical Significance and Assessment". imaging.onlinejacc.org. Retrieved 2016-02-12. 

  Physiology of the cardiovascular system Heart Cardiac output Cardiac cycle Cardiac output Heart rate Stroke volume Stroke volume End-diastolic volume End-systolic volume Afterload Preload Frank–Starling law of the heart Cardiac function curve Venous return curve Wiggers diagram Pressure volume diagram Ultrasound Fractional shortening = (End-diastolic dimension End-systolic dimension) / End-diastolic dimension Aortic valve area calculation Ejection fraction Cardiac index Heart rate Cardiac pacemaker Chronotropic (Heart rate) Dromotropic (Conduction velocity) Inotropic (Contractility) Bathmotropic (Excitability) Lusitropic (Relaxation) Conduction Conduction system Cardiac electrophysiology Action potential cardiac atrial ventricular Effective refractory period Pacemaker potential Electrocardiography P wave PR interval QRS complex QT interval ST segment T wave U wave Hexaxial reference system Chamber pressure Central venous Right atrial ventricular pulmonary artery wedge Left atrial ventricular Aortic Other Ventricular remodeling Vascular system/ Hemodynamics Blood flow Compliance Vascular resistance Pulse Perfusion Blood pressure Pulse pressure Systolic Diastolic Mean arterial pressure Jugular venous pressure Portal venous pressure Regulation of BP Baroreflex Kinin–kallikrein system Renin–angiotensin system Vasoconstrictors Vasodilators Autoregulation Myogenic mechanism Tubuloglomerular feedback Cerebral autoregulation Paraganglia Aortic body Carotid body Glomus cell