Perspectives on the History of Coronary Physiology: Discovery of Major Principles and Their Clinical Correlates.

Coronary circulation plays an essential role in delivering oxygen and metabolic substrates to satisfy the considerable energy demand of the heart. This article reviews the history that led to the current understanding of coronary physiology, beginning with William Harvey's revolutionary discovery of systemic blood circulation in the 17th century, and extending through the 20th century when the major mechanisms regulating coronary blood flow (CBF) were elucidated: extravascular compressive forces, metabolic control, pressure-flow autoregulation, and neural pathways. Pivotal research studies providing evidence for each of these mechanisms are described, along with their clinical correlates. The authors describe the major role played by researchers in the 19th century, who formulated basic principles of hemodynamics, such as Poiseuille's law, which provided the conceptual foundation for experimental studies of CBF regulation. Targeted research studies in coronary physiology began in earnest around the turn of the 20th century. Despite reliance on crude experimental techniques, the pioneers in coronary physiology made groundbreaking discoveries upon which our current knowledge is predicated. Further advances in coronary physiology were facilitated by technological developments, including methods to measure phasic CBF and its regional distribution, and by biochemical discoveries, including endothelial vasoactive molecules and adrenergic receptor subtypes. The authors recognize the invaluable contribution made by basic scientists toward the understanding of CBF regulation, and the enormous impact that this fundamental information has had on improving clinical diagnosis, decision-making, and patient care.

Balancing carcinoid crisis and right ventricular dysfunction during tricuspid and pulmonic valve replacement for carcinoid heart disease: A case report.

INTRODUCTION AND IMPORTANCE: Carcinoid tumors are rare malignancies of neuroendocrine origin that can manifest with a constellation of systemic symptoms including right-sided cardiac involvement. Many patients with carcinoid heart disease require valve replacement, but intraoperative management of carcinoid syndrome varies within the literature. CASE PRESENTATION: A 72-year-old man with carcinoid syndrome underwent tricuspid and pulmonic valve replacement with multiple episodes of carcinoid crisis intraoperatively as well as right ventricular dysfunction after cardiopulmonary bypass. CLINICAL DISCUSSION: Octreotide is the mainstay in prevention and treatment of intraoperative carcinoid crisis, but reported dosages and timing varies significantly. The use of exogenous catecholamines is also controversial as they are thought to paradoxically worsen carcinoid symptoms. Our patient was managed successfully with both an octreotide infusion and intermittent boluses, as well as exogenous catecholamines for right ventricular support during and after cardiopulmonary bypass. CONCLUSION: The management of carcinoid syndrome in patients undergoing valve surgery for carcinoid heart disease is dependent on timely prevention and treatment of carcinoid crisis and effective mitigation of right ventricular dysfunction.

A two-circuit strategy for intraoperative extracorporeal support during single lung transplantation in a patient bridged with venovenous extracorporeal membrane oxygenation.

Venovenous extracorporeal membrane oxygenation is increasingly used as a bridging strategy in decompensating patients awaiting lung transplantation. Various approaches for continuing support intraoperatively have been previously described. A two-circuit strategy that uses the in situ venovenous extracorporeal membrane oxygenation circuit supplemented with peripheral cardiopulmonary bypass allows for diversion of native cardiac output away from the transplanted lung as well as seamless continuation of venovenous extracorporeal membrane oxygenation postoperatively.

Hydroxocobalamin for treatment of catecholamine-resistant vasoplegia during liver transplantation: A single-center series of 20 cases.

INTRODUCTION: Catecholamine-resistant vasoplegia is a potentially devastating complication during liver transplantation. Hydroxocobalamin has emerged as a treatment for vasoplegia associated with cardiac surgery, liver transplantation, and septic shock. PRESENTATION OF CASE: We performed a retrospective review of patients who underwent liver transplantation between October 2015 and May 2020 to evaluate the efficiency of hydroxocobalamin in this setting. DISCUSSION: A total of 137 patients underwent liver transplantation, of which 20 received hydroxocobalamin for vasoplegia. Administration of hydroxocobalamin increased mean arterial pressure and reduced vasoactive drug requirements. CONCLUSION: This case series adds to the previous individual reports describing the use of hydroxocobalamin during liver transplantation suggesting hydroxocobalamin can mitigate refractory hypotension from catecholamine resistant vasoplegia during liver transplantation.

Blockade of endothelial Mas receptor restores the vasomotor response to phenylephrine in human resistance arterioles pretreated with captopril and exposed to propofol.

BACKGROUND: Hypotension that is resistant to phenylephrine is a complication that occurs in anesthetized patients treated with angiotensin converting enzyme (ACE) inhibitors. We tested the hypothesis that Ang 1-7 and the endothelial Mas receptor contribute to vasodilation produced by propofol in the presence of captopril. METHODS: The internal diameters of human adipose resistance arterioles were measured before and after administration of phenylephrine (10-9 to 10-5 M) in the presence and absence of propofol (10-6 M; added 10 min before the phenylephrine) or the Mas receptor antagonist A779 (10-5 M; added 30 min before phenylephrine) in separate experimental groups. Additional groups of arterioles were incubated for 16 to 20 h with captopril (10-2 M) or Ang 1-7 (10-9 M) before experimentation with phenylephrine, propofol, and A779. RESULTS: Propofol blunted phenylephrine-induced vasoconstriction in normal vessels. Captopril pretreatment alone did not affect vasoconstriction, but the addition of propofol markedly attenuated the vasomotor response to phenylephrine. A779 alone did not affect vasoconstriction in normal vessels, but it restored vasoreactivity in arterioles pretreated with captopril and exposed to propofol. Ang 1-7 reduced the vasoconstriction in response to phenylephrine. Addition of propofol to Ang 1-7-pretreated vessels further depressed phenylephrine-induced vasoconstriction to an equivalent degree as the combination of captopril and propofol, but A779 partially reversed this effect. CONCLUSIONS: Mas receptor activation by Ang 1-7 contributes to phenylephrine-resistant vasodilation in resistance arterioles pretreated with captopril and exposed to propofol. These data suggest an alternative mechanism by which refractory hypotension may occur in anesthetized patients treated with ACE inhibitors.

Left hemothorax resulting from delayed right ventricular apical pacing lead perforation without hemopericardium, a case report.

INTRODUCTION AND IMPORTANCE: Right ventricular pacemaker lead perforation is a rare but well documented complication of pacemaker implantation. Lead perforation can cause an array of symptoms ranging from none to hemodynamic instability and tamponade. In previously reported cases, lead perforation has always been able to be confirmed by imaging, with computed tomography (CT) scan considered to be the gold standard diagnostic imaging modality. CASE PRESENTATION: An 80-year-old male underwent uncomplicated implantation of a dual chamber pacemaker for sick sinus syndrome as an outpatient. Thirty-nine days later, the patient presented to the emergency department complaining of new-onset, left-sided, pleuritic chest pain. He was found to have unilateral hemothorax and abnormal pacemaker lead interrogation. Pacemaker lead perforation was suspected but not confirmed with imaging. Lead perforation was only identified after surgical exploration. CLINICAL DISCUSSION: This patient had multiple risk factors for pacemaker lead perforation. However, imaging, including CT scan was unable to confirm perforation. The presence of an otherwise unexplained left hemothorax strongly suggested that surgical intervention was indicated. The lead perforation was subsequently confirmed with subxiphoid exploration of the pericardial space. The mechanism of lead perforation resulting in hemothorax in this case is not straight forward, as no direct communication between the pericardial and pleural spaces was identified. However, previously described visceral pericardial self-sealing may contribute to the small pericardial accumulation described herein. CONCLUSION: This patient's presentation and clinical course underscore the importance of maintaining a high index of suspicion for pacemaker lead perforation despite a lack of confirmation with imaging.