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Hypertension, or high blood pressure, is a major risk factor for the development of left ventricular hypertrophy (LVH), which is characterized by thickening of the myocardium (heart muscle). LVH occurs in response to increased afterload (the resistance the heart has to pump against), which is a common feature of hypertension.

Angiotensin II, a hormone that is activated in response to hypertension, is a major mediator of LVH in this setting. Angiotensin II causes vasoconstriction (narrowing of blood vessels) and promotes the retention of salt and water, which increases blood volume and pressure. Additionally, angiotensin II stimulates the proliferation of cardiac myocytes (heart muscle cells) and the synthesis of extracellular matrix proteins, leading to hypertrophy and fibrosis of the myocardium.

Other factors that may contribute to LVH in hypertension include increased sympathetic nervous system activity, oxidative stress, and inflammation. However, angiotensin II is considered a key mediator of this process, and drugs that block the renin-angiotensin-aldosterone system (RAAS), such as angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), are often used to treat hypertension and reduce the risk of LVH and other cardiovascular complications.

Modifiable risk factors for coronary artery disease (CAD) are those that can be changed or controlled to reduce the risk of developing CAD. These include high blood pressure, high cholesterol levels, smoking, physical inactivity, unhealthy diet, and obesity. High HDL (high-density lipoprotein) is actually a desirable factor, as it is known as the "good cholesterol" and helps to remove excess cholesterol from the body. Orthostatic hypotension, or a drop in blood pressure upon standing, is not considered a modifiable risk factor for CAD.