Subject(s)
Coronary Artery Bypass , Coronary Vessels , Myocardial Infarction , Percutaneous Coronary Intervention , Postoperative Complications , Risk Assessment/methods , Coronary Artery Bypass/methods , Coronary Artery Bypass/mortality , Coronary Vessels/diagnostic imaging , Coronary Vessels/pathology , Humans , Multimorbidity , Myocardial Infarction/complications , Myocardial Infarction/mortality , Myocardial Infarction/therapy , Patient Care Management/methods , Percutaneous Coronary Intervention/methods , Percutaneous Coronary Intervention/mortality , Postoperative Complications/classification , Postoperative Complications/etiology , Postoperative Complications/mortality , Research Design , Risk Factors , Ventricular Function, LeftABSTRACT
Coronary microvascular resistance is increasingly measured as a predictor of clinical outcomes, but there is no accepted gold-standard measurement. We compared the diagnostic accuracy of 2 invasive indices of microvascular resistance, Doppler-derived hyperemic microvascular resistance (hMR) and thermodilution-derived index of microcirculatory resistance (IMR), at predicting microvascular dysfunction. A total of 54 patients (61 ± 10 years) who underwent cardiac catheterization for stable coronary artery disease (n = 10) or acute myocardial infarction (n = 44) had simultaneous intracoronary pressure, Doppler flow velocity and thermodilution flow data acquired from 74 unobstructed vessels, at rest and during hyperemia. Three independent measurements of microvascular function were assessed, using predefined dichotomous thresholds: (1) coronary flow reserve (CFR), the average value of Doppler- and thermodilution-derived CFR; (2) cardiovascular magnetic resonance (CMR) derived myocardial perfusion reserve index; and (3) CMR-derived microvascular obstruction. hMR correlated with IMR (rho = 0.41, p <0.0001). hMR had better diagnostic accuracy than IMR to predict CFR (area under curve [AUC] 0.82 vs 0.58, p <0.001, sensitivity and specificity 77% and 77% vs 51% and 71%) and myocardial perfusion reserve index (AUC 0.85 vs 0.72, p = 0.19, sensitivity and specificity 82% and 80% vs 64% and 75%). In patients with acute myocardial infarction, the AUCs of hMR and IMR at predicting extensive microvascular obstruction were 0.83 and 0.72, respectively (p = 0.22, sensitivity and specificity 78% and 74% vs 44% and 91%). We conclude that these 2 invasive indices of coronary microvascular resistance only correlate modestly and so cannot be considered equivalent. In our study, the correlation between independent invasive and noninvasive measurements of microvascular function was better with hMR than with IMR.
Subject(s)
Angina, Stable/diagnostic imaging , Angina, Stable/physiopathology , Echocardiography, Doppler , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/physiopathology , Vascular Resistance/physiology , Aged , Blood Flow Velocity/physiology , Cardiac Catheterization , Cardiac Output/physiology , Coronary Circulation/physiology , Female , Humans , Hyperemia/diagnostic imaging , Hyperemia/etiology , Hyperemia/physiopathology , Male , Microcirculation/physiology , Middle Aged , Sensitivity and Specificity , ThermodilutionABSTRACT
Background Cold air inhalation during exercise increases cardiac mortality, but the pathophysiology is unclear. During cold and exercise, dual-sensor intracoronary wires measured coronary microvascular resistance ( MVR ) and blood flow velocity ( CBF ), and cardiac magnetic resonance measured subendocardial perfusion. Methods and Results Forty-two patients (62±9 years) undergoing cardiac catheterization, 32 with obstructive coronary stenoses and 10 without, performed either (1) 5 minutes of cold air inhalation (5°F) or (2) two 5-minute supine-cycling periods: 1 at room temperature and 1 during cold air inhalation (5°F) (randomized order). We compared rest and peak stress MVR , CBF , and subendocardial perfusion measurements. In patients with unobstructed coronary arteries (n=10), cold air inhalation at rest decreased MVR by 6% ( P=0.41), increasing CBF by 20% ( P<0.01). However, in patients with obstructive stenoses (n=10), cold air inhalation at rest increased MVR by 17% ( P<0.01), reducing CBF by 3% ( P=0.85). Consequently, in patients with obstructive stenoses undergoing the cardiac magnetic resonance protocol (n=10), cold air inhalation reduced subendocardial perfusion ( P<0.05). Only patients with obstructive stenoses performed this protocol (n=12). Cycling at room temperature decreased MVR by 29% ( P<0.001) and increased CBF by 61% ( P<0.001). However, cold air inhalation during cycling blunted these adaptations in MVR ( P=0.12) and CBF ( P<0.05), an effect attributable to defective early diastolic CBF acceleration ( P<0.05) and associated with greater ST -segment depression ( P<0.05). Conclusions In patients with obstructive coronary stenoses, cold air inhalation causes deleterious changes in MVR and CBF . These diminish or abolish the normal adaptations during exertion that ordinarily match myocardial blood supply to demand.
Subject(s)
Blood Flow Velocity/physiology , Cold Temperature , Coronary Circulation/physiology , Coronary Stenosis/physiopathology , Coronary Vessels/physiopathology , Electrocardiography , Oxygen Consumption/physiology , Cardiac Catheterization , Coronary Angiography , Coronary Stenosis/diagnosis , Exercise Test/methods , Female , Follow-Up Studies , Humans , Magnetic Resonance Imaging, Cine , Male , Middle Aged , Retrospective StudiesSubject(s)
Acute Coronary Syndrome/complications , Cardiovascular System/physiopathology , Cold Temperature , Cold-Shock Response , Exercise , Myocardial Infarction/etiology , Acute Coronary Syndrome/diagnosis , Acute Coronary Syndrome/physiopathology , Acute Coronary Syndrome/therapy , Adaptation, Physiological , Animals , Energy Metabolism , Exercise Tolerance , Humans , Myocardial Infarction/diagnosis , Myocardial Infarction/metabolism , Myocardial Infarction/physiopathology , Myocardial Infarction/prevention & control , Myocardium/metabolism , Oxygen Consumption , Risk FactorsABSTRACT
The phenomenon of warm-up angina was first noted over 200 years ago. It describes the curious observation whereby exercise-induced ischaemia on second effort is significantly reduced or even abolished if separated from first effort by a brief rest period. However, the precise mechanism via which this cardio-protection occurs remains uncertain. Three possible explanations for reduced myocardial ischaemia on second effort include: first, an improvement in myocardial perfusion; second, increased myocardial resistance to ischaemia similar to ischaemic preconditioning; and third, reduced cardiac work through better ventricular-vascular coupling. Obtaining accurate coronary physiological measurements in the catheter laboratory throughout exercise demands a complex research protocol. In the 1980s, studies into warm-up angina relied on great cardiac vein thermo-dilution to estimate coronary blood flow. This technique has subsequently been shown to be inaccurate. However exercise physiology in the catheter laboratory has recently been resurrected with the advent of coronary artery wires that allow continuous measurement of distal coronary artery pressure and blood flow velocity. This review summarises the intriguing historical background to warm-up angina, and provides a concise critique of the important studies investigating mechanisms behind this captivating cardio-protective phenomenon.
ABSTRACT
The phenomenon of warm-up angina was first noted over 200 years ago. It describes the curious observation whereby exercise-induced ischaemia on second effort is significantly reduced or even abolished if separated from first effort by a brief rest period. However, the precise mechanism via which this cardio-protection occurs remains uncertain. Three possible explanations for reduced myocardial ischaemia on second effort include: first, an improvement in myocardial perfusion; second, increased myocardial resistance to ischaemia similar to ischaemic preconditioning; and third, reduced cardiac work through better ventricular-vascular coupling. Obtaining accurate coronary physiological measurements in the catheter laboratory throughout exercise demands a complex research protocol. In the 1980s, studies into warm-up angina relied on great cardiac vein thermo-dilution to estimate coronary blood flow. This technique has subsequently been shown to be inaccurate. However exercise physiology in the catheter laboratory has recently been resurrected with the advent of coronary artery wires that allow continuous measurement of distal coronary artery pressure and blood flow velocity. This review summarises the intriguing historical background to warm-up angina, and provides a concise critique of the important studies investigating mechanisms behind this captivating cardio-protective phenomenon.