Ventricular remodeling
In
Physiological remodeling is reversible while pathological remodeling 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.[3][4][5]
Ventricular remodeling may include
Pathophysiology
The
After a myocardial infarction (MI), cardiac myocyte death can be triggered by
Besides, the cardiac interstitium which consisted of largely Type I and Type III collagen fibres are also involved in cardiac remodeling. Cardiac collagen is synthesized by fibroblasts and degraded by metalloproteinases.
Other factors such as high blood pressure, activation of sympathetic system which releases norepinephrine, activation of renin–angiotensin system which releases renin and anti-diuretic hormones are important contributors of cardiac remodelling. However, atrial natriuretic peptide is thought to be cardio-protective.[7]
Evaluation
Remodeling of the heart is evaluated by performing an echocardiogram. The size and function of the atria and ventricles can be characterized using this test.[citation needed]
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.[9] Carvedilol, a 3rd generation beta blocker, may actually reverse the remodeling process by reducing left ventricular volumes and improving systolic function.[10][11] Cardiac resynchronization therapy (CRT) has shown the ability to reverse left ventricular remodeling in some patients.[12][13] 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.[citation needed]
See also
References
- PMID 18427637.
- ^ Ventricular+remodeling at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- PMID 16144994.
- PMID 19195605.
- PMID 12084610.
- PMID 23810323.
- ^ a b c d e Cohn, Jay N; Colucci, Wilson S; Yeon, Susan B. "Cardiac remodeling: Basic aspects". UpToDate.com. Retrieved 8 November 2017.
- ^ PMID 26647721.
- PMID 12668699.
- PMID 12783070.
- PMID 26131706.)
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: CS1 maint: multiple names: authors list (link - PMID 25190241.
- PMID 16401777.
Further reading
- "Left Ventricular Remodeling in Heart Failure: Current Concepts in Clinical Significance and Assessment". imaging.onlinejacc.org. Retrieved 2016-02-12.