Sequence and magnitude of ventricular volume changes in painful and painless myocardial ischemia.

Abstract

Stimulation of left ventricular stretch receptors has been proposed as a possible mechanism for the occurrence of cardiac pain. Changes in left ventricular volume were continuously assessed in 12 patients during 11 spontaneous (two painful) and 12 ergometrine-induced (nine painful) ischemic attacks with a precordial scintillation probe and blood pool labeling with technetium99m. In all ischemic episodes, spontaneous or induced, painful or painless, severe dilatation of the left ventricle was consistently observed. These changes always preceded the onset of ST segment shifts and occurred long before pain, when present. The Activation of mechanoreceptors by bulging of the ischemic area12,13 has also been proposed as a mechanism potentially responsible for cardiac pain. To check this hypothesis, we have explored the possibility that the magnitude or the rate of change of left ventricular volume during acute myocardial ischemia, or a combination of these parameters, could account for the presence or absence of anginal pain.

Impaired left ventricular filling rate induced by treatment with recombinant interleukin 2 for advanced cancer.

“…In all cases the hypokinesia affected the anteroseptal wall and was associated with reduction in peak emptying and filling rates and ejection fraction. Although these changes were associated with ST-T alterations in only two patients they resemble the pattern of left ventricular function impairment seen during ischaemia.29 30 This suggests the possibility that in some patients with latent coronary artery disease rIL-2 may reduce regional coronary flow and hence cause myocardial ischaemia and regional wall motion abnormalities. Clinical studies are needed to assess changes in myocardial perfusion after in vivo rIL 2 administration.…”

A Study of Clinical Profile of Unrecognised Myocardial Infarction

“…Potential stimuli include mechanical factors such as ischaemia-induced changes in the tone of the ventricular wall and chemical factors released by cardiac myocytes in response to hypoxia. (4,5) One such mediator is adenosine, which has been shown to reproduce chest pain in patients with angina. (6) In addition, evidence suggests that the size of the myocardial infarction is important; larger infarctions induce greater discomfort.…”

Bedside assessment of myocardial performance in the critically ill

“…The importance of changes in diastolic function has been demonstrated in both ischaemic heart disease and sepsis [15]. Measurement of ejection fraction using these techniques has been validated in a number of clinical settings; for diagnostic use in ischaemic heart disease [78,79], for continuous ambulatory monitoring of left ventricular function, in the moni-toring of vasodilator therapy [80,81], pre-, post-and during angioplasty [82], and pre-and post-cardiac surgery [83]. The principal disadvantages of these techniques are the necessity of labelling the red blood cells with radioisotope (99m-technetium), the limited duration of the labelling allowing typically 8 h of monitoring after each labelling.…”