Heart transplant can be considered as the “gold standard” treatment for end-stage heart failure, with nearly 5.7 million adults in the United States carrying a diagnosis of heart failure. According to the International Society for Heart and Lung Transplantation registry, nearly 3300 orthotopic heart transplants were performed in 2016 in North America. In spite of significant improvements in overall perioperative care of heart transplant recipients for the past few decades, the risk of 30-day mortality remains 5% to 10%, primarily related to early failure of the allograft. Early graft dysfunction (EGD) occurs within 24 hours after transplant, manifesting as left ventricular dysfunction, right ventricular dysfunction, or biventricular dysfunction. EGD is further classified into primary and secondary graft dysfunction. This review focus on describing overall incidences of EGD, potential risk factors associated with EGD, perioperative preventive measures, and various management options.
Patients with obstructive sleep apnea (OSA) have increased cardiovascular disease risk largely attributable to hypertension. Heightened peripheral chemoreflex sensitivity (i.e., exaggerated responsiveness to hypoxia) facilitates hypertension in these patients. Nitric oxide blunts the peripheral chemoreflex and patients with OSA have reduced nitric oxide bioavailability. We therefore investigated the dose-dependent effects of acute inorganic nitrate supplementation (beetroot juice), an exogenous nitric oxide source, on blood pressure and cardiopulmonary responses to hypoxia in patients with OSA using a randomized, double-blind, placebo-controlled crossover design. Fourteen patients with OSA (53±10years, 29.2±5.8kg/m2, apnea-hypopnea index=17.8±8.1, 43%F) completed three visits. Resting brachial blood pressure, as well as cardiopulmonary responses to inspiratory hypoxia, were measured before, and two hours after, acute inorganic nitrate supplementation (~0.10mmol [placebo], 4.03mmol [low-dose], and 8.06mmol [high-dose]). Placebo did not increase either plasma [nitrate] (30±52 to 52±23μM, P=0.26) or [nitrite] (266±153 to 277±164nM, P=0.21); however, both increased following low-(29±17 to 175±42μM, 220±137 to 514±352nM) and high-doses (26±11 to 292±90μM, 248±155 to 738±427nM, respectively, P<0.01 for all). Following placebo, systolic blood pressure increased (120±9 to128±10mmHg, P<0.05) whereas no changes were observed following low-(121±11 to 123±8mmHg, P=0.19) or high-dose (124±13 to 124±9mmHg, P=0.96). The peak ventilatory response to hypoxia increased following placebo (3.1±1.2 to 4.4±2.6L/min, P<0.01) but not low-(4.4±2.4 to 5.4±3.4L/min, P=0.11) or high-doses (4.3±2.3 to 4.8±2.7L/min, P=0.42). Inorganic nitrate did not change the heart rate responses to hypoxia (beverage-by-time P=0.64). Acute inorganic nitrate supplementation appears to blunt an early-morning rise in systolic blood pressure potentially through suppression of peripheral chemoreflex sensitivity in patients with OSA.
Prolonged ischemia can result in cellular dysfunction. Paradoxically, the reintroduction of blood flow (reperfusion) can lead to further damage, described as ischemia-reperfusion injury (I/R). It has been reported that I/R attenuates endothelial function at the micro- and macrovascular level. An attenuation in microvascular endothelial function from I/R may therefore disrupt the ability to modulate exercise hyperemia in contracting skeletal muscle. We tested the hypothesis that I/R blunts the rapid and steady-state hyperemic and vasodilatory response to rhythmic handgrip exercise. Ten young healthy subjects (8M/2F; 24 ± 1 yr) completed two separate study visits (I/R and time control trials) in a random order. On each study visit rapid-onset hyperemia and vasodilation following a single forearm contraction was assessed in duplicate. Rhythmic handgrip exercise (20 contractions per min) was then completed for 3 min. All handgrip exercises were performed at 20% maximum voluntary contraction. Following exercise, either I/R was induced (pneumatic cuff placed around the upper left arm at 240 mmHg for 20 min followed by 20 min of reperfusion) or a time control trial (supine rest for 40 min) was completed. Handgrip exercises were then repeated immediately after each respective intervention. Brachial artery blood velocity and diameter were measured with Doppler ultrasound and forearm vascular conductance (FVC) was calculated as forearm blood flow (FBF; ml·min-1) over blood pressure (mmHg). In response to a single muscle contraction, peak hyperemia (ΔFBF from baseline) and vasodilation (ΔFVC) were attenuated following I/R (134 ± 15 vs. 103 ± 13 ml·min-1; 160 ± 17 vs. 118 ± 15 ml·min-1·100 mmHg-1, P<0.05 for both) but not following time control (115 ± 20 vs. 124 ± 18 ml·min-1; 150 ± 25 vs. 148 ± 20 ml·min-1·100 mmHg-1, P=0.16 and P=0.95, respectively). Total FBF and FVC following a single muscle contraction was not different between I/R (25 ± 4 vs. 20 ± 3 ml; 33 ± 5 vs. 24 ± 4 ml·100 mmHg-1) and time control (21 ± 4 vs. 23 ± 4 ml; 28 ± 5 vs. 28 ±4 ml·100 mmHg-1) trials (group x time interactions P=0.05 and P=0.08, respectively). Steady-state ΔFBF and ΔFVC during rhythmic exercise was unchanged in both I/R (192 ± 16 vs. 190 ± 17 ml·min-1; 208 ± 18 vs. 193 ± 19 ml·min-1·100 mmHg-1) and time control (188 ± 17 vs. 196 ± 15 ml·min-1; 206 ± 19 vs. 207 ± 15 ml·min-1·100 mmHg-1) trials (group x time interactions P=0.34 and 0.21, respectively). Our data indicate that 40 min of I/R blunts hyperemia and vasodilation at the onset of skeletal muscle contraction, but does not appear to attenuate these responses during steady-state rhythmic exercise. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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