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Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice
Published on: April 13, 2015
[Hemodynamics in ischemia: diastolic phase]
Insights
Acute ischemia impairs diastolic function by slowing ventricular relaxation and delaying filling. This impacts the heart
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Context:
- The cardiac cycle's diastolic phase involves complex relaxation and filling processes.
- Left ventricular diastolic function depends on intrinsic myocardial properties and extrinsic factors.
- Diastole is crucial for adequate cardiac output and myocardial perfusion.
Purpose:
- To elucidate the mechanisms by which acute ischemia affects left ventricular diastolic function.
- To detail the physiological alterations in diastolic phases due to ischemia.
- To describe the measurable parameters indicating impaired diastolic function.
Summary:
- Diastole comprises isovolumic relaxation, rapid and slow filling, and atrial contraction.
- Ischemia disrupts diastolic function by slowing isovolumic relaxation and delaying ventricular filling.
- Key indicators of impaired diastolic function include reduced peak negative dP/dt, increased time constant (T), and altered filling rates.
Impact:
- Understanding ischemic effects on diastolic function is vital for diagnosing and managing cardiac conditions.
- Identifies specific physiological changes that can be monitored non-invasively.
- Highlights the energy-dependent nature of myocardial relaxation and its vulnerability to ischemia.
Abstract:
The diastolic portion of the cardiac cycle can be divided into sequential phases: isovolumic ventricular relaxation; rapid ventricular filling; slow, or passive, ventricular filling; and atrial contraction. Contraction and relaxation are to some extent interrelated; however, relaxation is not simply a passive reversal of events during systole. Rather, relaxation is an energy-consuming process which involves dissociation of calcium from the actin-myosin-complex and reuptake of calcium by the sarcoplasmic reticulum. Left ventricular diastolic function is determined by the interrelationship of several/factors, including some intrinsic to the left ventricular chamber (completeness of left ventricular relaxation, time course of left ventricular contraction, and elastic and viscous properties of the myocardium) and others extrinsic to the left ventricle (pericardial and pleural pressure, right ventricular contraction, and coronary perfusion pressure). Acute ischemia alters diastolic left ventricular function by: slowing isovolumic relaxation, delaying left ventricular filling and altering passive elastic properties of the myocardium. Slowing of isovolumic relaxation is measured as a fall in the maximal rate of left ventricular pressure decline (peak negative dP/dt) and as an increase in the time constant (T) of left ventricular pressure fall. Delayed left ventricular filling is manifested regionally as a reduced rate of septal and posterior wall thinning (by echocardiography) and globally as a reduced rate of chamber filling (by gated radionuclide angiography).(ABSTRACT TRUNCATED AT 250 WORDS)
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