How does hypertension cause atherosclerosis

Hollander W. Role of hypertension in atherosclerosis and cardiovascular disease. The American Journal of Cardiology. American Heart Association Journals. Alexander RW. Hypertension and the pathogenesis of atherosclerosis: oxidative stress and the mediation of arterial inflammatory response: a new perspective.

American College of Cardiology. Updated May 7, Kannel WB. Hypertension: reflections on risks and prognostication. Medical Clinics of North America. Harvard Health. Atherosclerosis, what is it? Updated April, American Heart Association.

What is cardiac catheterization? Updated July 31, Exercise stress test. Medications for treating hypertension. Updated August Your Privacy Rights. To change or withdraw your consent choices for VerywellHealth. At any time, you can update your settings through the "EU Privacy" link at the bottom of any page.

These choices will be signaled globally to our partners and will not affect browsing data. We and our partners process data to: Actively scan device characteristics for identification. I Accept Show Purposes. Table of Contents View All. Table of Contents. What Is Atherosclerosis? Hypertension and Atherosclerosis.

Arteries in the brain: This can lead to a stroke or transient ischemic attack. Arteries in the lower extremities or abdomen: This is referred to as peripheral artery disease. Arteries in the kidneys: This can lead to kidney disease or kidney failure. The Spiraling Affect of Hypertension and Atherosclerosis Atherosclerosis may be a consequence of hypertension, but once atherosclerosis occurs, hypertension will almost invariably worsen. Was this page helpful?

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Why Is My Cholesterol High? What to Know About Inspra Eplerenone. This would result in a reduced release of endothelium-derived relaxing factor which is known to be a potent vasodilator, inhibits proliferation of vascular smooth muscle cells, endothelial movement and extracellular matrix production.

Medial thickening by proliferation of smooth muscle cells and perivascular fibrosis were observed. When coronary hypertension is combined with hypertrophy, as is often the case in systemic arterial hypertension, the two remodelling processes described are superimposed. Experimental data show that after relief of pressure overload there is a regression of medial hypertrophy and perivascular collagen, first at larger arterial microvessels and then in small microvessels 17 but perivascular collagen deposition may remain.

Either due to coronary atherosclerosis or to a decreased coronary reserve, clinical manifestations of CHD angina, myocardial infarction are frequent in hypertensive patients. Resting electrocardiogram show alterations of repolarisation suggestive of ischaemia and exercise tests may have a false-positive response.

Ischaemia may also contribute to produce subendocardial fibrosis which in turn contribute to diastolic as well as to systolic dysfunction. It has been suggested that acute coronary syndromes might be favoured by an increased flow velocity and shear stress which could contribute to plaque disruption. It has been shown in hypertensive patients with normal coronary arteries that flow velocity is increased which is only partially reversed by isosorbide.

In hypertensives with left ventricular hypertrophy the risk of reinfarction, overall mortality and mortality due to CHD are significantly increased. It is important to emphasise that treatment of hypertension reduces significantly the number of fatal and non-fatal cardiovascular events in patients with CHD.

General principles for the treatment of hypertension fully apply to patients with hypertension and CHD. Vasodilator agents may cause reflex stimulation of baroreceptors and tachycardia and increased contractility resulting in increased myocardial oxygen demand and thus aggravating angina.

On that respect, hydralazine or short-acting calcium antagonists should be avoided. Global evaluation of the patient is mandatory. It is important to evaluate the extension of organic damage, the presence of diabetes and other risk factors, and the presence of aggravating factors such as thyrotoxicosis and anaemia, etc, and obviously the severity and extension of coronary disease.

Non-pharmacologic and pharmacologic treatment must be linked to reduce overall cardiovascular risk. Furthermore stabilisation of atherosclerotic plaque is of extreme importance.

Antithrombotic agents, as well as statins when necessary, are important on these grounds. All other therapeutic considerations to treat CHD should be considered including revascularisation procedures. Assmann G, Schulte H. Scandivanian Simvastatin Survival Study group.

Randomized trial of cholesterol lowering in patients with coronary artery disease: the Scandinavian Simvastatin Survival Study 4 S Lancet : — Sacks FM et al. The effect of pravastatin on coronary events after myocardial infarction inpatients with average cholesterol levels: the cholesterol and recurrent events CARE trial N Engl J Med : — Prevention of cardiovascular events and death with pravastatin inpatients with coronary heart disease and a broad range of initial cholesterol levels N Engl J Med : — Blood pressure, systolic and diastolic, and cardiovascular risks.

US population data Arch Int Med : — MacMahon S et al. Blood pressure,stroke and coronary heart disease. Part 1. Prolonged differences in blood pressure: prospective observational studies corrected for the regression dilution bias Lancet : — O'Donell CJ et al.

Hypertension and borderlineisolated systolic hypertension increase risks of cardiovascular disease and mortality in male physicians Circulation 95 : — Article Google Scholar. Exacerbation of atherosclerosis by hypertension. Potential mechanisms and clinical implications Arch Int Med : — Insulin resistance.

A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia and atherosclerotic cardiovascular disease Diabetes Care 14 : — Strauer BE. The concept of coronary flow reserve J Cardiovasc Pharmacol 19 Suppl 5 : 67— Chilian WM et al. Thyroxine-induced left ventricular hypertrophy in the rat: anatomical and physiological evidence for angiogenesis Cir Res 57 : — People with chest pain who arrive by ambulance usually receive faster treatment at the hospital, too.

Our online community of survivors and caregivers is here to keep you going no matter the obstacles. Written by American Heart Association editorial staff and reviewed by science and medicine advisers. See our editorial policies and staff. High Blood Pressure. Understanding Blood Pressure Readings. Blood Pressure Toolkit. The damage can build over time The excess strain and resulting damage from high blood pressure HBP or hypertension causes the coronary arteries serving the heart to slowly become narrowed from a buildup of fat, cholesterol and other substances that together are called plaque.