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It is important that the medical profession play a significant role in critically evaluating the use of diagnostic procedures and therapies as they are introduced in the detection, management,

/pdf/acc-aha-2006-guidelines-for-the-management-of-patients-with-27qfh9fc7i.pdf

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease

2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons

https://cdr.lib.unc.edu/downloads/4m90dx441

ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease)

When the heart faces a hemodynamic burden, it can do the following to compensate: (1) use the Frank-Starling mechanism to increase crossbridge formation; (2) augment muscle mass to bear the extra load; and (3) recruit neurohormonal mechanisms to increase contractility. The first mechanism is limited in its scope, and the third is deleterious as a chronic adjustment. Thus, increasing mass assumes a key role in the compensation for hemodynamic overload. This increase in mass is due to the hypertrophy of existing myocytes rather than hyperplasia, because cardiomyocytes become terminally differentiated soon after birth. In response to pressure overload in conditions such as aortic stenosis or hypertension, the parallel addition of sarcomeres causes an increase in myocyte width, which in turn increases wall thickness. This remodeling results in concentric hypertrophy (increase in ratio of wall thickness/chamber dimension).

According to LaPlace’s Law, the load on any region of the myocardium is given as follows: (pressure×radius)/(2×wall thickness); thus, an increase in pressure can be offset by an increase in wall thickness. Because systolic stress (afterload) is a major determinant of ejection performance, the normalization of systolic stress helps maintain a normal ejection fraction even when needing to generate high levels of systolic pressure.1 Volume overload in conditions such as chronic aortic regurgitation, mitral regurgitation, or anemia engenders myocyte lengthening by sarcomere replication in series and an increase in ventricular volume. This pattern of eccentric hypertrophy (cavity dilatation with a decrease in ratio of wall thickness/chamber dimension) is also initially compensatory, such that the heart can meet the demand to sustain a high stroke volume. However, chronic hypertrophy may be deleterious because it increases the risk for the development of heart failure and premature death.

This review will focus on the pathogenesis of pressure- versus volume-overload types of left ventricular hypertrophy (LVH), detection, …

Left Ventricular Hypertrophy Pathogenesis, Detection, and Prognosis

http://www.saudident.com/album/data/media/2/valvular_heart_disease.pdf

ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease)

The cause of reduced ejection performance in patients with aortic stenosis is controversial. The relative contribution of afterload and contractility was evaluated in 76 patients with pure or predominant valvular aortic stenosis studied by left ventricular micromanometry and quantitative cineangiography. Thirteen patients without detectable heart disease served as controls. The ejection performance was assessed in terms of the mean normalized systolic ejection rate (MNSER, normal 2 2.0 end-diastolic volumes (EDV)/sec), contractility by total pressure Vmax (normal 2 1.47 muscle lengths/sec) and/or peak measured velocity of shortening (normal 1.14 muscle lengths/sec) and afterload by peak systolic circumferential wall stress (normal < 460 dyn. 10′/cm2).The patients were divided into four groups according to the level of isovolumic contractility and peak systolic wall stress. In group 1, contractility and wall stress were normal. In group 2, contractility was normal and wall stress was increased. Wall stress was normal in group 3 and increased in group 4; in both groups, the isovolumic contractile indexes were depressed. At normal (groups 1 and 3) or increased (groups 2 and 4) wall stress, MNSER was significantly (p < 0.01) smaller in patients with reduced isovolumic contractility (1.72 EDV/sec in group 3 and 1.48 EDV/sec in group 4) than in the corresponding groups with normal contractility (2.34 EDV/sec in group 1 and 2.13 EDV/sec in group 2). Conversely, with a normal (control group and groups 1 and 2) or depressed (groups 3 and 4) contractile state, there was a significant inverse linear relationship between MNSER and systolic wall stress. The slopes of the two curves were almost identical, but the intercept on the y-axis (MNSER) was significantly (p < 0.001) smaller in patients with depressed contractility (3.09 EDV/sec) than in those with normal contractility (2.59 EDV/sec). Thus, both altered contractility and increased afterload are operative in depressing left ventricular ejection performance.The observation that contractile state can be normal or impaired at normal and increased systolic wall stress is evidence for nonuniform myocardial quality in adequate as well as inadequate hypertrophy. The significantly higher left ventricular angiographic muscle mass in groups 3 and 4 than in groups 1 and 2 is consistent with the concept that whether or not hypertrophy is adequate or inadequate in terms of maintaining normal systolic stress, advanced myocardial hypertrophy leads to depression of contractility.

Determinants of ejection performance in aortic stenosis.

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Determinants of ejection performance in aortic stenosis.