Pathophysiology of Cardiovascular Diseases

Pathophysiology of Cardiovascular Diseases

  • Cellular and Molecular Mechanisms of Cardiovascular Dysfunction
  • Hemodynamic and Structural Changes
  • Neurohormonal Regulation
  • Metabolic and Genetic Factors
  • Cellular Remodeling and Fibrosis
  • Mechanisms of Electrical and Conduction System Abnormalities
  • Systemic Inflammation and Immunologic Contributions
  • Blood Vessel Dysfunction and Microcirculatory Abnormalities

The pathophysiology of cardiovascular diseases involves complex processes that disrupt the normal function of the heart and blood vessels. A key mechanism is atherosclerosis, where plaque builds up in the arteries, leading to narrowing and hardening of the blood vessels, ultimately reducing blood flow. This decreased flow results in ischemia, a condition where tissues are deprived of oxygen, increasing the risk of heart attacks or strokes. Hypertension, or high blood pressure, contributes to the problem by placing excessive stress on the walls of blood vessels, which promotes inflammation and endothelial dysfunction, further complicating the disease process. Heart failure occurs when the heart is no longer able to pump blood effectively, which can result from weakened cardiac muscles in systolic heart failure or stiffened ventricles in diastolic heart failure. Arrhythmias, or abnormal heart rhythms, arise from disruptions in the heart’s electrical impulses, leading to irregular heartbeats and compromised cardiac function. At the cellular level, oxidative stress, inflammation, and apoptosis exacerbate tissue damage, promoting disease progression. Additionally, genetic mutations can predispose individuals to certain cardiomyopathies or congenital heart defects, further complicating the clinical picture. Understanding these underlying mechanisms is essential for the development of targeted therapies aimed at halting or reversing disease progression. These advancements hold promise in not only managing CVDs but potentially offering ways to repair damaged tissues and restore normal heart function, thus improving patient outcomes and quality of life.

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Committee Members

Professor
Lu Cai

University of Louisville School of Medicine, United States

Professor
Terry McCormack

Hull York Medical School, United Kingdom

Consultant Cardiologist
Abdul Majeed Salmasi

London Northwest University Healthcare NHS Trust, United Kingdom

Professor
Bernd Blobel

University of Regensburg, Germany

CVS 2026 Speakers

Professor
Emre Yalcinkaya

University of Health Sciences, Turkey

Professor
Guo Wei He

Tianjin University, China

Professor
Gausal Azam Khan

King Faisal University, Saudi Arabia

Researcher
Hai Tao Hou

Tianjin University, China

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