Hypertensive heart disease: risk factors, complications and mechanisms

Figures

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  Figure 1. Effect of chronic hemodynamic stress on the heart. Chronic hypertension resulting from various stimuli leads to left ventricular hypertrophy as a compensation for the hemodynamic stress and metabolic demand on the heart. However, heart failure results when the heart can no longer withstand the persistent hemodynamic stress. BP, blood pressure.

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  Figure 2. Angiotensin II formation and effects on blood pressure. Angiotensinogen is produced by the liver and converted to angiotensin I by the action of renin produced by the juxtaglomerular cells of the kidney. Angiotensin I is then converted to angiotensin II via angiotensin-converting enzyme (ACE). Angiotensin II binds to its receptors to induce several activities such as inflammation, vasoconstriction oxidative stress and reabsorption of water and sodium leading to elevated blood pressure and hypertension; MAS, marker assisted selected.

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  Figure 3. Electrocardiography and conduction system of the heart. (A) Normal Electrocardiography (ECG). (B) Conduction system of the heart. (C) Atrial Fibrillation ECG tracing.

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  Figure 4. Atherosclerosis progression in coronary artery disease. (A) Coronary artery disease is characterized by narrowed coronary arteries due to advanced atherosclerotic fatty plaque. (B) Atherosclerosis in coronary artery disease and complications. Atherosclerosis is initiated by fatty streak and macrophage infiltration to rid of cholesterol deposits in the coronary arteries. Macrophages that have engulfed cholesterol deposits transform into lipid laden foam cells, enter the subendothelial layer and also activate the immune system leading to inflammation. Increased deposition of fat, calcium and persistent inflammation leads to formation of fibrotic and calcic changes that can result in plaque rupture, thrombosis and blockage of blood flow in the vasculature. The resulting complications of advanced atherosclerotic lesions include myocardial infarction, atrial fibrillation and left ventricular hypertrophy among others. Activated macrophages and T cells are the main players.

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  Figure 5. Salt induced hypertension. In high salt environments, dendritic cells or macrophages become activated through increased intracellular sodium that enter via the epithelial sodium channel (ENaC). Sodium activates NADPH oxidase and the inflammasome leading to formation of Isolevuglandins(IsoLGs)-protein adducts that are processed in major histocompatibility molecules and presented to T cells, activating them. Activated T cells produce inflammatory cytokines IFN-γ, TNF-α and IL-17A that lead to hypertension. NF-Kb, Nuclear factor kappa-light-chain-enhancer of activated B cells; IFN-γ, interferon gamma; TNF-α, Tumor necrosis factor alpha; ROS, reactive oxygen species; NLRP3, NACHT, LRR, and PYD domains-containing protein 3; ASC, Apoptosis-associated speck-like protein containing a CARD.