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Diastolic pressure-volume relations in the diseased heart
Insights
Diastolic dysfunction in the heart, common in diseases like coronary artery disease and cardiomyopathy, involves altered ventricular properties. Research suggests physiological factors and contractile element interactions contribute to this diastolic stiffness.
Area of Science:
- Cardiology
- Physiology
Background:
- Ventricular diastolic properties are altered in various heart diseases, including coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy.
- Acute increases in left ventricular (LV) diastolic pressure during ischemia may cause dyspnea and pulmonary congestion.
- The mechanisms of altered diastolic distensibility are debated, with evidence supporting residual diastolic interaction between contractile elements in ischemic hearts.
Purpose of the Study:
- To explore alterations in ventricular diastolic properties in diseased hearts.
- To investigate the contribution of physiological factors and contractile interactions to diastolic stiffness.
Main Methods:
- Review of existing evidence on diastolic dysfunction in coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy.
- Analysis of studies examining the effects of ischemia, sodium nitroprusside, and salbutamol on LV diastolic properties.
Main Results:
- Congestive cardiomyopathy is associated with increased LV diastolic stiffness, potentially influenced by fibrosis and physiological factors.
- Left ventricular hypertrophy (LVH) shows increased effective diastolic chamber stiffness, with normalized stiffness elevated only in chronic pressure overload LVH.
- Transient ischemia during angina pectoris involves acute increases in LV diastolic pressure, possibly due to contractile element interactions.
Conclusions:
- Physiological factors and residual diastolic interactions play significant roles in diastolic stiffness in various heart conditions.
- Understanding these mechanisms is crucial for managing heart diseases characterized by diastolic dysfunction.
Abstract:
Alterations in ventricular diastolic properties are commonly seen in the diseased heart, and have been extensively studied in coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy due to pressure or volume overload. Acute increases in left ventricular (LV) diastolic pressure relative to volume occur regularly during the transient ischemia of angina pectoris and may contribute to the dyspnea and pulmonary congestion that commonly accompany this condition. Although the mechanism of this altered disastolic distensibility is debated, a substantial body of evidence favors a role for residual diastolic interaction between contractile elements in the ischemic heart. Congestive cardiomyopathy also appears to be associated with increased LV diastolic stiffness. While this may in part be related to fibrosis of the LV wall, shifts of the abnormal diastolic pressure-volume relation toward normal have been reported with sodium nitroprusside infusion or the beta-adrenergic agonist salbutamol, suggesting important contribution of physiologic factors to the increased resting LV stiffness in this condition. LV hypertrophy (LVH) is associated with increased effective diastolic chamber stiffness, but normalized LV diastolic stiffness is increased only in LVH due to chronic pressure overload. Possible explanations for these findings are discussed.