INTRODUCTION
In diastolic heart failure, the left ventricular ejection fraction (LVEF) is normal and the dominant functional abnormality resides in diastole. Thus, there is increased passive stiffness with impaired relaxation of the ventricle, which results in a disturbed pattern of left ventricular (LV) filling and elevated end diastolic pressure. Global systolic performance, function, and contractility remain normal. However, several reports indicate that abnormalities in regional shortening are present in patients with diastolic heart failure. These findings have been interpreted as evidence supporting the notion that heart failure is somehow caused by these regional abnormalities in shortening. The significance of these observations, particularly their relation to the syndrome of heart failure, remains uncertain. Accordingly, in this chapter we will review the published data on LV global and regional systolic function in diastolic heart failure and will attempt to reconcile what appear to be disparate conclusions about LV systolic function in patients with this condition.
PATHOPHYSIOLOGY
The term diastolic dysfunction refers to an abnormality of LV diastolic distensibility, filling, or relaxation—regardless of whether the EF is normal or abnormal and whether the patient is asymptomatic or symptomatic with clinical evidence of heart failure. In the absence of symptoms, those with a normal EF and diastolic dysfunction are said to have preclinical heart disease or asymptomatic diastolic dysfunction. Patients with the signs and symptoms of heart failure, a normal LVEF, and LV diastolic dysfunction are said to have diastolic heart failure. If nonmyocardial causes of heart failure (e.g., mitral stenosis) are excluded, such patients meet published criteria for diastolic heart failure. Thus, diastolic heart failure refers to a syndrome of heart failure that is not caused by reduced systolic function, but rather is closely related to chronic structural remodeling and abnormalities in the diastolic properties of the left ventricle. These definitions of asymptomatic diastolic dysfunction and diastolic heart failure parallel those used in asymptomatic and symptomatic patients with LV systolic dysfunction and facilitate the use of a pathophysiologic, diagnostic, and therapeutic framework that includes all patients with LV dysfunction.
Cardiac Structure and Diastolic Function
The anatomic features of hearts from patients with diastolic heart failure differ substantially from those with systolic heart failure ( Table 28-1 ) (see Chapter 2 ). Patients with diastolic heart failure generally exhibit a concentric pattern of LV remodeling and a hypertrophic process that is characterized by a normal or near-normal end diastolic volume and increased wall thickness with a high ratio of mass-to-volume and a high ratio of wall thickness-to-chamber radius ( Table 28-2 ). At the microscopic level, the cardiomyocyte exhibits an increased diameter, and there is an increase in the amount of collagen surrounding the myocytes. These anatomic or structural features tend to parallel abnormalities in diastolic function.
| DIASTOLIC HF | SYSTOLIC HF | |
|---|---|---|
| Clinical Features | ||
| Symptoms (e.g., dyspnea) | Yes | Yes |
| Congestive state (e.g., edema) | Yes | Yes |
| Exercise tolerance | Decreased | Decreased |
| Neurohormonal activation (e.g., BNP) | Yes | Yes |
| LV Structure and Geometry | ||
| LV mass and geometry | Concentric LVH | Eccentric LVH |
| Relative wall thickness | Increased | Decreased |
| End diastolic volume | Normal | Increased |
| Cardiomyocytes | Increased diameter | Increased length |
| Extracellular matrix | Increased collagen | Decreased collagen |
| NORMAL | DHF | p | |
|---|---|---|---|
| LV end diastolic volume (ml) | 115 ± 9 | 103 ± 22 | <0.001 |
| LV end systolic volume (ml) | 45 ± 12 | 45 ± 11 | NS |
| LV mass (g) | 164 ± 35 | 251 ± 101 | <0.001 |
| Relative wall thickness | 0.38 ± 0.06 | 0.53 ± 0.11 | <0.001 |
| Systolic blood pressure (mmHg) | 128 ± 8 | 160 ± 40 | <0.001 |
| LV systolic wall stress (g/cm 2 ) | 201 ± 32 | 187 ± 44 | NS |
The passive elastic properties of the ventricle and the process of active relaxation determine the LV diastolic pressure-volume (P-V) relation and diastolic function. Abnormal passive elastic properties are caused largely by increased myocardial mass and alterations in the extramyocardial collagen network, but changes in intramyocardial components (e.g., titin) also contribute to an increase in passive stiffness. The effects of abnormally prolonged or delayed myocardial relaxation can be superimposed on the passive diastolic P-V curve and cause a further increase in diastolic pressure relative to volume. Those changes in passive stiffness, relaxation, or both produce an upward displacement of the diastolic P-V relation, and as a result, chamber compliance is reduced, the time course of filling is altered, and LV diastolic pressure is elevated. Under these circumstances a relatively small increase in central blood volume or an increase in venous and arterial tone can cause a substantial increase in left atrial (LA) and pulmonary venous pressures (i.e., diastolic heart failure).
Contractile Behavior
A comprehensive description of the systolic or contractile behavior of the left ventricle requires measurement of LV performance, function, and contractility, as well as a consideration of ventricular remodeling and loading conditions and a distinction between global and regional properties.
Global Contractile Behavior
The functional capacity of the whole ventricle is most appropriately described by a composite of parameters reflecting LV performance, function, and contractility. Such parameters are determined using a combination of cardiac catheterization and imaging techniques.
Performance
The pumping ability or performance of the left ventricle is best described by the stroke work, which credits the ventricle for pressure and volume work in a single integrated index. This index of performance is determined as the product of developed pressure and total stroke volume. Thus it becomes obvious that it may be increased in hypertensive patients or decreased in patients with a small LV chamber and a low stroke volume. However, stroke work is normal in the vast majority of patients with diastolic heart failure ( Fig. 28-1 and Table 28-3 ). It should be recognized that this performance index reflects a pumping property of the whole ventricle, not that of a unit of myocardium. Indeed, if the value for stroke work is expressed relative to LV mass, work may be subnormal. Thus, myocardial performance (work per gram of myocardium) may be abnormal in patients with LV hypertrophy (LVH), but the pump performance (stroke work) of the whole ventricle remains normal.
| NORMAL | DHF | p | |
|---|---|---|---|
| LV Systolic Performance | |||
| SW (kg-cm) | 8.8 ± 2.5 | 8.4 ± 2.3 | NS |
| LV Systolic Function | |||
| SW/EDV (g/cm 2 ) | 74 ± 10 | 81 ± 14 | <0.01 |
| PRSW (g/cm 2 ) | 109 ± 18 | 99 ± 22 | NS |
| Fractional shortening (%) | 33 ± 5 | 27 ± 4 | NS |
| Ejection fraction (%) | 0.61 ± 0.07 | 0.58 ± 0.06 | NS |
| Vcf (circumferences/sec) | 1.8 ± 0.2 | 1.8 ± 0.2 | NS |
| PEP/LVET | 0.37 ± 0.19 | 0.35 ± 0.13 | NS |
| LV Contractility | |||
| Peak (+)dP/dt (mmHg/s) | 1664 ± 305 | 1596 ± 362 | NS |
| ESP/ESV (mmHg/ml) | 2.1 ± 0.8 | 2.6 ± 1.1 | <0.05 |
| Ees (mmHg/ml) | 1.6 ± 0.5 | 2.4 ± 0.9 | <0.001 |
| E es < (mmHg/g) | 1.2 ± 0.4 | 1.1 ± 0.6 | NS |
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
