Abstract 16976: Derangements in Cardiac Oxidative Metabolism in Humans With Dilated Cardiomyopathy

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel Clark ◽  
Giovanni E Davogustto ◽  
Susan P Bell ◽  
RAVINDER MALLUGARI ◽  
William S Bradham ◽  
...  
Keyword(s):  
Myocardial Perfusion ◽  
Dilated Cardiomyopathy ◽  
Oxidative Metabolism ◽  
Myocardial Perfusion Reserve ◽  
Normal Subjects ◽  
Rate Pressure Product ◽  
Gadolinium Contrast ◽  
Perfusion Reserve ◽  
Demand Rate ◽  
Myocardial Oxidative Metabolism

Introduction: Dilated cardiomyopathy (DCM) is associated with impaired myocardial perfusion reserve and impaired myocardial oxidative metabolism. However, the association between myocardial perfusion reserve and oxidative metabolism, is not fully understood. Hypothesis: Reduced myocardial perfusion reserve is associated with reduced myocardial oxidative metabolism. Methods: Using non-invasive cardiac imaging, we studied 8 DCM patients and 14 normal subjects. Myocardial perfusion reserve index (MPRI) was calculated using cardiac magnetic resonance as the normalized rate of myocardial signal augmentation following gadolinium contrast injection between rest and regadenoson induced stress. Resting oxidative metabolism was calculated as the myocardial mono-exponential decay rate (Kmono) of [ 11 C]acetate by positron emission tomography normalized per unit demand (rate-pressure product, RPP) (Kmono/RPP). Results: MPRI was lower in DCM compared to controls (1.25 ± 0.22 vs 1.59 ± 0.49, p=0.038). Similarly, Kmono/RPP was lower in DCM compared with normal subjects (0.6x10e-3 ± 0.15 x10e-3 vs 1.2x10e-3 ± 0.9x10e-3, p<0.0001). There was a linear relation between Kmono and RPP in normal subjects. However, DCM patients showed no increase in Kmono regardless of RPP (Figure 1A). Kmono/RPP was not significantly related to MPRI in either group (Figure 1B). Conclusions: Patients with DCM exhibit markedly impaired myocardial oxidative metabolism compared to normal subjects. However, this impairment was not quantitatively related to impaired myocardial perfusion reserve. Of the various mechanisms that could explain decrease in oxidative metabolism in DCM, these data suggest that reduced myocardial perfusion is not the principal driver of impaired oxidative metabolism.

Myocardial perfusion reserve and oxidative metabolism contribute to exercise capacity in patients with dilated cardiomyopathy

2004 ◽  
Vol 10 (2) ◽  
pp. 132-140 ◽  
Author(s):  
Kira Q. Stolen ◽  
Jukka Kemppainen ◽  
Kari K. Kalliokoski ◽  
Kirsti Hällsten ◽  
Matti Luotolahti ◽  
...  
Keyword(s):  
Myocardial Perfusion ◽  
Dilated Cardiomyopathy ◽  
Exercise Capacity ◽  
Oxidative Metabolism ◽  
Myocardial Perfusion Reserve ◽  
Perfusion Reserve

Myocardial perfusion reserve in adults with cyanotic congenital heart disease

2005 ◽  
Vol 289 (5) ◽  
pp. H1798-H1806 ◽  
Author(s):  
Richard C. Brunken ◽  
Joseph K. Perloff ◽  
Johannes Czernin ◽  
Roxana Campisi ◽  
Susan Purcell ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Myocardial Perfusion ◽  
Congenital Heart ◽  
Myocardial Perfusion Reserve ◽  
Cyanotic Congenital Heart Disease ◽  
Rate Pressure Product ◽  
Perfusion Reserve ◽  
Positron Emission ◽  
Perfusion Measurements

In patients with cyanotic congenital heart disease (CCHD), a right-to-left shunt results in systemic hypoxemia. Systemic hypoxemia incites a compensatory erythrocytosis, which increases whole blood viscosity. We considered that these changes might adversely influence myocardial perfusion in CCHD patients. Basal and hyperemic (intravenous dipyridamole) perfusion measurements were obtained with [13N]ammonia positron emission tomographic imaging in left (LV) and right (RV) ventricular and septal myocardium in 14 adults with CCHD [age: 34.1 yr (SD 6.5)]; hematocrit: 62.2% (SD 4.8)] and 10 healthy controls [age: 34.1 yr (SD 6.5)]. In patients, basal perfusion measurements were higher in LV [0.77 (SD 0.24) vs. 0.55 ml·min−1·g−1 (SD 0.09), P < 0.02], septum [0.71 (SD 0.16) vs. 0.49 ml·min−1·g−1 (SD 0.09), P < 0.001], and RV [0.77 (SD 0.30) vs. 0.38 ml·min−1·g−1 (SD 0.09), P < 0.001]. However, basal measurements normalized for the rate-pressure product were similar to those of controls. Calculated oxygen delivery relative to rate-pressure product was higher in the patients [2.2 (SD 0.8) vs. 1.6 (SD 0.4) × 10−5 ml O2·min−1·g tissue−1·(beats·mmHg)−1 in the LV, P < 0.05, and 2.0 (SD 0.7) vs. 1.4 (SD 0.3) × 10−5 ml O2·min−1·g tissue−1·(beats·mmHg)−1 in the septum, P < 0.01]. Hyperemic perfusion measurements in CCHD patients did not differ from controls [LV, 1.67 (SD 0.60) vs. 1.95 ml·min−1·g−1 (SD 0.46); septum, 1.44 (SD 0.56) vs. 1.98 ml·min−1·g−1 (SD 0.69); RV, 1.56 (SD 0.56) vs. 1.65 ml·min−1·g−1 (SD 0.64), P = not significant], and coronary vascular resistances were comparable [LV, 55 (SD 25) vs. 48 mmHg·ml−1·g·min (SD 16); septum, 67 (SD 35) vs. 50 mmHg·ml−1·g·min (SD 21); RV, 59 (SD 26) vs. 61 mmHg·ml−1·g·min (SD 27), P = not significant]. These findings suggest that adult CCHD patients have remodeling of the coronary circulation to compensate for the rheologic changes attending chronic hypoxemia.

Epicardial coronary stenosis severity and myocardial perfusion

2020 ◽  
pp. 12-16
Keyword(s):  
Myocardial Perfusion ◽  
Myocardial Ischemia ◽  
Coronary Disease ◽  
Myocardial Perfusion Reserve ◽  
Pharmacological Intervention ◽  
Fractional Flow ◽  
Perfusion Reserve ◽  
Flow Reserve ◽  
Stenosis Severity ◽  
Microvascular Resistance

Patients suspected of having epicardial coronary disease are often investigated with noninvasive myocardial ischemia tests to establish a diagnosis and guide management. However, the relationship between myocardial ischemia and coronary stenoses is affected by multiple factors, and there is marked biological variation between patients. The ischemic cascade represents the temporal sequence of pathophysiological events that occur after interruption of myocardial oxygen delivery. The earliest part of the cascade is examined via perfusion imaging, and fractional flow reserve (FFR) is a corresponding index which is specific to the coronary artery. Whereas FFR has come to be regarded a clinical reference standard against which other newer invasive and noninvasive tests are validated, the diagnostic FFR threshold for detecting ischemia was established against a combination of noninvasive ischemia tests that assessed different stages of the ischemic cascade. Moreover, the validity of invasive pressure-derived indices of stenosis severity are contingent on the assumption that pressure is proportional to flow if microvascular resistance is constant, a condition induced by pharmacological intervention or by examining specific segments of the cardiac cycle. Furthermore, myocardial perfusion reserve depends on dynamic modulation of microvascular resistance, and dysfunction of the microvasculature can lead to ischemia even in the absence of epicardial coronary disease.

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