Left ventricular hypertrophy is associated with worse survival independent of ventricular function and number of coronary arteries severely narrowed

Cooper, Richard S.; Simmons, Brian E.; Castañer, Angel; Santhanam, Vimala; Ghali, Jalal K.; Mar, Maxine

doi:10.1016/0002-9149(90)90807-d

Cited by 177 publications

(64 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The interaction of these two pathologies is the likely cause of the higher sudden death rates in young, black adults. 18 …”

Section: Hypertensionmentioning

confidence: 99%

Epidemiology and burden of cardiovascular disease

Watkins

2004

Clin Cardiol

View full text Add to dashboard Cite

Summary: Coronary heart disease (CHD) is the leading cause of death in the United States. The rate of CHD and CHD death varies across racial groups, with higher rates among black men and women than among white men and women. The development of CHD is promoted by major CHD risk factors-dyslipidemia, hypertension, and smoking. These risk factors are independently associated with CHD risk and are common among adults in the United States. Diabetes mellitus is also a significant contributor to CHD risk and is associated with risk of a CHD event equivalent to that conferred by the presence of prior CHD. Metabolic syndrome, a related condition, also confers a high risk for CHD as well as for the development of type 2 diabetes. Diabetes and metabolic syndrome are characterized by the presence of central obesity and insulin resistance, which result in dyslipidemia, hypertension, and cardiovascular derangements that promote CHD. Diabetes and metabolic syndrome illustrate the significance of risk factor clustering, which contributes to CHD risk through the additive effect of each risk factor. Diabetes, metabolic syndrome, and risk factor clustering in general are becoming more prevalent, which illustrates the need for better CHD prevention strategies aimed at risk factor control. The pathologic process associated with risk factor clustering also contributes to the higher CHD burden among black men and women, who have a higher prevalence of risk factor clustering and type 2 diabetes. Furthermore, despite having a higher CHD risk, black men and women are less likely to receive adequate treatment or control of risk factors, including dyslipidemia or hypertension. Eliminating disparities among population groups will thus require aggressive efforts focused on risk assessment, guideline adherence, and risk factor control in populations in need.

show abstract

“…The interaction of these two pathologies is the likely cause of the higher sudden death rates in young, black adults. 18 …”

Section: Hypertensionmentioning

confidence: 99%

Epidemiology and burden of cardiovascular disease

Watkins

2004

Clin Cardiol

View full text Add to dashboard Cite

show abstract

“…[3][4][5] In the heart, complex changes occur, including the remodeling of intramyocardial coronary arterioles 6 and accumulation of fibrillar collagen in the perivascular adventitia and interstitium of the myocardium. [7][8][9] As a consequence of these changes, the myocardium becomes abnormally stiff and ventricular function is reduced.…”

mentioning

confidence: 99%

Differential Effects of Angiotensin II on Cardiac Cell Proliferation and Intramyocardial Perivascular Fibrosis In Vivo

et al. 1998

View full text Add to dashboard Cite

Background-Growth effects of angiotensin II (Ang II) contribute to cardiac remodeling. Remodeling, in turn, may be influenced by proliferation of nonmyocytes. The aims of this study were to determine in vivo which cardiac cell types proliferate in response to Ang II, to evaluate whether proliferation is mediated by the Ang II AT 1 receptor, and to establish whether blood pressure affects cell proliferation by comparing proliferation in the normotensive right atrium and ventricle and pressure-overloaded left ventricle. Methods and Results-Groups of 8 Wistar rats were implanted with miniosmotic pumps releasing 5-bromo-2Ј-deoxyuridine (BrdU) as a cell proliferation marker for 2 weeks. Two groups received Ang II infusions via a second minipump and drinking waterϮlosartan. Two groups received vehicleϮlosartan. Cell proliferation was assessed as the percentage of nuclei that incorporated BrdU. Ang II increased proliferation within medial vascular smooth muscle cells (VSMCs) and in associated adventitial/interstitial fibroblasts of intramyocardial coronary arterioles but decreased proliferation of myoendothelial cells. Despite increased blood pressure, proliferation in atria and ventricles was similar. Aldosterone levels were not significantly elevated, suggesting direct proliferative effects of Ang II. Losartan reduced Ang II-induced VSMC and adventitial fibroblast proliferation but had no effect on myoendothelial cell proliferation. Conclusions-These results indicate direct, differential effects of Ang II on proliferation of atrial and ventricular nonmyocytes. VSMC and fibroblast proliferation is AT 1 receptor-dependent, whereas myoendothelial cells are controlled by an AT 1 -independent mechanism. The effects are independent of aldosterone and blood pressure and have important implications in renin-dependent hypertension and chronic cardiac failure when circulating Ang II is elevated.

show abstract

“…3 Collectively, these changes in coronary resistance vessels serve to reduce their ratio of wall thickness to lumen and adversely influence their capacity for vasodilatation. 21 An interstitial fibrosis is another feature of the adverse structural remodeling of the myocardium found in HHD.…”

mentioning

confidence: 99%

Structural remodeling in hypertensive heart disease and the role of hormones.

1994

View full text Add to dashboard Cite

In hypertension, the risk of adverse cardiovascular events, including heart failure, is increased in the presence of left ventricular hypertrophy. Morphological studies suggest that it is not the quantity but rather the quality, or structure, of myocardium that confers such risk. Iterations in tissue structure that appear in hypertensive heart disease include a remodeling of intramyocardial coronary arterioles, similar to that found in systemic organs, and a disproportionate accumulation of fibrillar collagen within their adventitia and neighboring interstitial space. Microscopic scars replacing necrotic cardiac myocytes are also evident. These expressions of fibrosis appear in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles and are linked to the renin-angiotensin-aldosterone system. Cardiac myocyte growth, the major determinant of myocardial mass, is related to ventricular loading. Mechanisms responsible for the reactive and reparative fibrosis with renin-angiotensin-aldosterone system activation are under investigation. In vitro quantitative autoradiography has identified angiotensin II, aldosterone, T he appearance of symptomatic heart failure and adverse cardiovascular events, such as myocardial infarction, sudden cardiac death, and stroke, occur with increased frequency in patients with systemic hypertension. For years, the pathophysiologica] basis for such increased risk has been presumed to be solely related to elevated arterial pressure. More recently, emphasis in conferring risk has been placed on the structural remodeling of the cardiovasculature. For example, in patients with uncomplicated hypertension, risk has been linked to left ventricular hypertrophy (LVH). 13 Viewed not as a separate organ but as an integral component of the cardiovasculature, the heart and its intramyocardial coronary arteries and arterioles participate in a structural remodeling that involves systemic organs as well. 48 The remodeling of systemic arterioles accounts for hypertension. The heart in turn responds to enhanced ventricular loading with a hypertrophic growth of cardiac myocytes, and accordingly, left ventricular mass is increased. The diffuse nature of the structural remodeling process, involving the right and left ventricles and systemic organs, suggests a role for circulating substances or substances produced locally within cardiovascular tissue. In this connection, it is noteworthy that risk has also been linked to an activation of the renin-angiotensin-aldosterone system (RAAS). endothelin, and bradykinin receptors in the myocardium. A nonendothelial tissue angiotensin-converting enzyme, whose binding density is marked in the matrix of heart valves, adventitia, and sites of fibrosis, irrespective of its pathogenic basis, has also been found. This angiotensin-converting enzyme may be responsible for regulating local concentrations of angiotensin II and bradykinin that govern fibroblast collagen turnover. Based on a paradigm of discordant reciprocal regulation, in wh...

show abstract

Left ventricular hypertrophy is associated with worse survival independent of ventricular function and number of coronary arteries severely narrowed

Cited by 177 publications

References 22 publications

Epidemiology and burden of cardiovascular disease

Epidemiology and burden of cardiovascular disease

Differential Effects of Angiotensin II on Cardiac Cell Proliferation and Intramyocardial Perivascular Fibrosis In Vivo

Structural remodeling in hypertensive heart disease and the role of hormones.

Contact Info

Product

Resources

About