Ventricular remodeling overview: Difference between revisions
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{{Ventricular remodeling}} | {{Ventricular remodeling}} | ||
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{{SK}} Left ventricular remodeling; LV remodeling | |||
==Overview== | ==Overview== | ||
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==Pathophysiology== | ==Pathophysiology== | ||
The [[cardiac myocyte]] is the major cell involved in remodeling. [[Fibroblast]]s, [[collagen]], the interstitium, and the [[coronary vessel]]s 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 scar formation 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. | |||
==Causes== | ==Causes== | ||
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==Treatment== | ==Treatment== | ||
Many factors influence the time course and extent of remodeling, including the severity of the insult, secondary events (recurrent ischemia or infarction),[[neurohormone|neurohormonal]] activation, genetic factors and [[gene expression]], and treatment. Medications may attenuate remodeling. [[ACE inhibitor|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. 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. | |||
==References== | ==References== | ||
Latest revision as of 18:21, 26 November 2013
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Ventricular Remodeling |
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Differentiating Ventricular Remodeling From Other Conditions |
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Diagnosis |
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Treatment |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Left ventricular remodeling; LV remodeling
Overview
Ventricular remodeling refers to the changes in size, shape, and function of the heart after injury to the left ventricle. 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.
Medically speaking, "ventricular remodeling" implies a decline in function (even though the word "remodeling" usually implies improvement). The term "reverse remodeling" in cardiology implies an improvement in ventricular mechanics and function after a remote injury.
Classification
Pathophysiology
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 scar formation 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.
Causes
Differentiating Ventricular Remodeling From Other Conditions
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Other Imaging Findings
Treatment
Many factors influence the time course and extent of remodeling, including the severity of the insult, 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. 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.