Left ventricular and vascular changes in valvular heart disease

Left ventricular hemodynamics: Pressure-volume loops

Familiarity with pressure-volume (PV) loops is foundational for understanding the LV response to stenosis or regurgitation of the mitral or aortic valves. Core concepts include preload, afterload, and contractility. Fig. 5.2 shows a generic PV loop, with labels describing each part of the loop and important lines.

Preload is the stretch of the sarcomeres in the myocardium at end-diastole before contraction. Preload is proportional to the volume of blood in the ventricle at end-diastole, but it is also influenced by the pressure required to achieve that volume. Preload is increased by increased blood volume or increased vasomotor tone in the venous system that increases blood return to the heart. An increase in preload, specifically an increase in end-diastolic volume, is associated with a rise in stroke volume if afterload and contractility remain constant ( Fig. 5.3 ).

In contrast, a decrease in preload is associated with a decrease in stroke volume (see Fig. 5.3 ). Pertinent to this chapter, valve disease that alters the normal flow of blood through and out of the heart may also increase LV end-diastolic volume (e.g., MR, aortic regurgitation [AR]). Moreover, changes in the diastolic properties of the heart may increase preload, even at the same end-diastolic volume. Hypertrophic remodeling that decreases the compliance of the heart shifts the end-diastolic PV curve, or compliance curve, upward and to the left, and for any given LV end-diastolic volume, the end-diastolic pressure is higher ( Fig. 5.4 ).

Afterload is the resistance to muscle fiber shortening during the systolic, or ejection, phase of the cardiac cycle. Muscle fiber tension, or wall stress, is quantified by the law of Laplace, which states that wall stress equals the intraventricular pressure multiplied by the radius of the LV cavity, divided by twice the thickness of the LV wall. Usually, the intraventricular pressure is essentially equal to aortic pressure. Increased pressure in the aorta (e.g., hypertension) and increased LV chamber dilation increase afterload, whereas an increase in wall thickness reduces wall stress and afterload.

On a PV loop, afterload, or arterial elastance, is represented by the line between the maximum LV end-diastolic point on the x-axis and the point of aortic valve closure at end-systole ( Fig. 5.5 ). An increase in the slope of this line reflects an increase in afterload, which is accompanied by a decrease in stroke volume for a given preload and contractility (see Fig. 5.5 ). In contrast, a decrease in the slope of the line, perhaps related to administration of a vasodilator, reflects a decrease in afterload, which is accompanied by an increase in stroke volume for a given preload and contractility (see Fig. 5.5 ). An LV outflow tract obstruction, such as AS, adds resistance to LV emptying. The pressure gradient across the obstructed valve yields a much higher intraventricular pressure than aortic pressure, contributing to higher wall stress that is magnified as the severity of valve stenosis progresses.

Contractility is the calcium-dependent ability of muscle to contract, or generate force, at a given fiber length. In terms of PV loops, the contractility of the ventricle as a whole is considered, and it may be altered by multiple factors, including inotropes, acidosis, and exercise. However, myocardial contractility may differ across the heart due to infarction, nonmyocyte infiltration, variation in electrical activation, and other regional differences. On a PV loop, contractility is represented by the line connecting the intersection of the x-axis and y-axis and the point representing end-systole (i.e., end-systolic PV line) ( Fig. 5.6 ). This is also referred to as end-systolic elastance .

For a given preload and afterload, an increase in contractility leads to a decrease in the LV end-systolic volume and a resulting increase in stroke volume (see Fig. 5.6 ). In contrast, a decrease in contractility is associated with an increase in end-systolic volume and decrease in stroke volume (see Fig. 5.6 ). For patients with valve disease, compensatory mechanisms in place that alter contractility to preserve hemodynamics in the face of increased afterload or preload may begin to fail over time, which may precede or accompany the clinical decline of the patient.

Left ventricular hypertrophic remodeling

The heart can undergo hypertrophic remodeling in response to a variety of stimuli. Depending on the stimulus, this hypertrophic growth may be partially or completely reversible. Hypertrophic growth can be adaptive, as in the case of exercise, or pathologic, as in the case of hypertrophic cardiomyopathy.

The four principal categories of hypertrophic remodeling are (1) normal geometry; (2) concentric remodeling; (3) concentric hypertrophy; and (4) eccentric hypertrophy ( Fig. 5.7 ). The patterns of hypertrophic remodeling associated with each left-sided valve lesion are shown in Fig. 5.7 . Numerous factors influence the type and degree of remodeling that may occur in a given individual, including age, sex, genetics, metabolic factors, coronary disease, and blood pressure. Pressure or volume overload, or both, from heart valve disease can have an important effect on hypertrophic remodeling of the LV.

Changes to the left ventricle with left-sided valve disease