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Heart Failure II: Pathophysiology

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...

Mitral Regurgitation I: Introduction

Mitral Regurgitation I: Introduction

Mitral regurgitation is characterized by the backward circulation of blood from the left ventricle to the left atrium during systole, a phase of the cardiac cycle when the heart contracts and pumps blood out of the chambers. This abnormal flow occurs primarily due to the dysfunction of the mitral valve or its supporting structures, which include the mitral leaflets, chordae tendineae, annulus, and papillary muscles.Etiology and Mechanisms:Primary Mitral Regurgitation: This type arises from...

Cardiomyopathy II: Dilated Cardiomyopathy

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Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...

Mitral Stenosis I: Introduction

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Pathophysiology of Heart Failure

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Updated: Jun 21, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

Left ventricular structural and functional changes in the metabolic syndrome.

Azra Mahmud¹, Ibrahim Almuntaser, Angie Brown

¹Department of Pharmacology and Therapeutics and Hypertension Clinic, Trinity College and St. James's Hospital, Dublin, Ireland. mahmuda@tcd.ie

Journal of the Cardiometabolic Syndrome

|July 21, 2009

Summary

Metabolic syndrome (MS) is linked to heart abnormalities like increased left ventricular thickness and reduced function, even when body mass index (BMI) is normal. These cardiac changes are independent of BMI.

Related Experiment Videos

Last Updated: Jun 21, 2026

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model

Published on: November 29, 2024

Area of Science:

Cardiology
Metabolic Diseases
Echocardiography

Background:

Metabolic syndrome (MS) is a cluster of conditions increasing cardiovascular risk.
Cardiac structural and functional changes are observed in MS, but their independence from body mass index (BMI) requires clarification.

Purpose of the Study:

To investigate whether cardiac abnormalities in metabolic syndrome are independent of body mass index (BMI).

Main Methods:

160 untreated patients underwent 2D echocardiography, tissue Doppler imaging, and MS evaluation.
Comparison of cardiac parameters between patients with and without MS, adjusting for age, BMI, and other determinants.

Main Results:

Patients with MS showed increased left ventricular relative wall thickness (RWT) and reduced midwall fractional shortening (MFS) and peak mitral annular velocity (Em) compared to controls.
A linear relationship existed between the number of MS features and Em velocity, RWT, and MFS.
MS was an independent predictor of reduced Em velocity, even after adjusting for age and left ventricular mass.

Conclusions:

Metabolic syndrome is associated with left ventricular concentric remodeling.
Reduced systolic (MFS) and diastolic (Em) function in MS are independent of BMI.
These findings highlight specific cardiac alterations in MS irrespective of obesity levels.