Why the study?
Does pacing-induced myocardial ischemia alter lung mechanics and left ventricular pressure-volume relations in patients with anginal syndrome?
Does pacing-induced myocardial ischemia alter lung mechanics and left ventricular pressure-volume relations in patients with anginal syndrome?
Myocardial ischemia acutely increases left ventricular end-diastolic pressure, leading to altered lung mechanics that may explain the sensation of chest tightness or breathlessness during angina.
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Ischemia may link LV pressure changes to dyspnea via lung mechanics; leaves open causal role and need for confirmation in larger studies.
The anginal syndrome (AP) typically includes sensations of chest tightness or difficulty in breathing. Left ventricular (LV) dysfunction during myocardial ischemia incident with AP is now well documented. Since secondary alterations in lung mechanics could relate to these symptoms, we examined airway resistance (Raw), lung volume (TGV), lung compliance (C L ), and LV pressure-volume relations during pacing-induced AP. LV end-diastolic pressure (EDP) increased suddenly with AP, (mean + 41%, p < 0.01), without change in end-diastolic volume (EDV). LV distensibility (EDV/EDP) decreased abruptly, (–37%, P < 0.01), with reduction in airway conductance (1/Raw/TGV), (–40%, P < 0.05), and C L (–27%, P < 0.05). When AP was relieved, these changes returned toward preangina levels. Ischemia-induced LV dysfunction abruptly increases LVEDP. The resulting increased pulmonary capillary pressure effects an alteration of lung mechanics consisting of increasing Raw and reduced C L . The changes in ventilatory effort which ensue may be interpreted as chest tightness, heaviness, or constriction by the AP patient.
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Pepine et al. (1972) studied this question.
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