Physical training improves myocardial perfusion but not left ventricular function response to exercise in patients with microvascular angina.

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Physical training improves myocardial perfusion but not left ventricular function response to exercise in patients with microvascular angina.

Q J Nucl Med Mol Imaging. 2017 Mar 16;:

Authors: Carvalho EE, Crescêncio JC, Santi GL, Oliveira LF, Schwartzmann PV, Gallo L, Marin-Neto JA, Simões MV

Abstract
BACKGROUND: Patients with primary microvascular angina (PMA) commonly exhibit abnormal left ventricular function (LVF) during exercise, potentially owing to myocardial ischemia. Herein, we investigated n PMA patients the effect of the reduction of myocardial perfusion disorders, by using aerobic physical training, upon LVF response to exercise.
METHODS: Overall, 15 patients (mean age, 53.7±8.9 years) with PMA and 15 healthy controls (mean age, 51.0±9.4 years) were studied. All subjects were subjected to baseline resting and exercise ventriculography, myocardial perfusion scintigraphy (MPS), and cardiopulmonary testing. PMA group members then participated in a 4-month physical training program and were reevaluated via the same methods applied at baseline.
RESULTS: Baseline left ventricular ejection fraction (LVEF) determinations by ventriculography were similar for both groups (PMA, 67.7±10.2%; controls, 66.5±5.4%; p=0.67). However, a significant rise in LVEF seen in control subjects during exercise (75.3±6.2%; p=0.0001) did not materialize during peak exercise in patients with PMA (67.7±10.2%; p=0.47). Of the 12 patients in the PMA group who completed the training program, 10 showed a significant reduction in reversible perfusion defects during MPS. Nevertheless, LVEF at rest (63.5±8.7%) and at peak exercise (67.3±15.9%) did not differ significantly (p=0.30) in this subset.
CONCLUSIONS: In patients with PMA, reduced left ventricular inotropic reserve observed during exercise did not normalize after improving myocardial perfusion through aerobic physical training.

PMID: 28299921 [PubMed - as supplied by publisher]

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