“…Furthermore, no unified hypotheses explain the mechanisms that underlie EISTE in Q wave leads. This ECG phenomenon has been attributed by various researchers to (a) wall motion abnormality [9, 10, 11, 16, 17, 18, 19, 20, 21], (b) myocardial ischemia [9, 10, 11, 12, 22, 23, 24], (c) both (a) and (b) [25, 26, 27, 28, 29], or (d) neither (a) nor (b) [30, 31, 32]. The failure of these explanations to encompass the full scope of the electrocardiographic and electrophysiologic mechanisms that underlie EISTE in Q wave leads inspired our critical review of this ECG phenomenon.…”
Most attempts to identify qualitative and quantitative techniques for assessing myocardial viability and the likelihood of improved function after revascularization in patients with healed myocardial infarcts have focused on treatment strategies and prognosis. This review examines the true value of the electrocardiographic phenomenon of exercise-induced ST segment elevation (EISTE) in Q wave leads as a diagnostic tool for the assessment of myocardial viability. The prognostic potential and clinical utility of the EISTE phenomenon are inhibited both by the heart’s electrophysiologic response to exercise-induced metabolic and hemodynamic changes, and by the ECG’s limited facility in assessing myocardial preservation. The use of EISTE as an independent indicator for surgical intervention is proscribed by these limitations. The EISTE phenomenon could serve as a useful tool in the first line of discrimination in patients with healed Q wave myocardial infarction, and may justify further diagnostic work-up in patients under consideration for a revascularization procedure. In the era of sophisticated nuclear and echo techniques, accurate imaging studies should not be replaced by ECG analysis alone in the search for viable tissue, except when financial costs are of major importance.
“…Furthermore, no unified hypotheses explain the mechanisms that underlie EISTE in Q wave leads. This ECG phenomenon has been attributed by various researchers to (a) wall motion abnormality [9, 10, 11, 16, 17, 18, 19, 20, 21], (b) myocardial ischemia [9, 10, 11, 12, 22, 23, 24], (c) both (a) and (b) [25, 26, 27, 28, 29], or (d) neither (a) nor (b) [30, 31, 32]. The failure of these explanations to encompass the full scope of the electrocardiographic and electrophysiologic mechanisms that underlie EISTE in Q wave leads inspired our critical review of this ECG phenomenon.…”
Most attempts to identify qualitative and quantitative techniques for assessing myocardial viability and the likelihood of improved function after revascularization in patients with healed myocardial infarcts have focused on treatment strategies and prognosis. This review examines the true value of the electrocardiographic phenomenon of exercise-induced ST segment elevation (EISTE) in Q wave leads as a diagnostic tool for the assessment of myocardial viability. The prognostic potential and clinical utility of the EISTE phenomenon are inhibited both by the heart’s electrophysiologic response to exercise-induced metabolic and hemodynamic changes, and by the ECG’s limited facility in assessing myocardial preservation. The use of EISTE as an independent indicator for surgical intervention is proscribed by these limitations. The EISTE phenomenon could serve as a useful tool in the first line of discrimination in patients with healed Q wave myocardial infarction, and may justify further diagnostic work-up in patients under consideration for a revascularization procedure. In the era of sophisticated nuclear and echo techniques, accurate imaging studies should not be replaced by ECG analysis alone in the search for viable tissue, except when financial costs are of major importance.
The human right ventricle has a relatively low tolerance to even short periods of ischemia. During angioplasty of the right coronary artery, pulmonary artery pressure typically rises due to an increase in right ventricular afterload caused by left ventricular dysfunction during ischemia. We have presented two cases of angioplasty in the early proximal portion of a large, highly dominant right coronary artery. Pulmonary artery and systemic pressure fell during balloon inflation probably secondary to acute severe right ventricular failure, though an interaction with left ventricular dysfunction cannot be excluded. These observations do emphasize the hemodynamic and combined ventricular consequences of proximal angioplasty in a large, dominant right coronary artery, particularly in the setting of preexisting left ventricular dysfunction.
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