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Irvine Page in the United States and Eduardo Braun-Menéndez in Argentina led teams of investigators that studied the role of the kidney in blood pressure regulation. Contemporaneously in 1939, each team using different methods discovered and described a new substance now known as angiotensin. At the time of discovery, Page called it "angiotonin" and Braun-Menéndez called it "hipertensina," anglicized to "hypertensin." Over time, the importance of this substance in circulatory control, pathophysiology and pharmacology became indisputable and the need for a single name became obvious. In a remarkable accommodation, Page and Braun-Menéndez agreed to forego any claim to priority and chose a name with elements of both. Following this compromise, Page and Braun-Menéndez went on to become leaders in science in their own countries as well as recognition world-wide while, angiotensin and its derivatives have become standard components in the understanding and treatment of diseases of the heart, kidney and brain., (Copyright © 2018 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.)

Background: Reciprocal ST-depression in the electrocardiograms (ECGs) of patients with ST-elevation myocardial infarction (STEMI) results from either true ischemia at a distance via collateral circulation diverting blood to the infarcted region or an electrical phenomenon that results from a mirror reflection of ST-elevation. We aimed to identify the role of reciprocal ECG changes in predicting collateral circulation to the infarcted area determined angiographically., Methods: In a retrospective study, ECG and angiography of 53 STEMI patients admitted to SUNY Upstate Medical University in 2014 were reviewed independently by experts blinded to the results of ECG and coronary angiography., Results: Reciprocal changes (RC) in ECG were present in 41 patients (77%) and on angiography, 14 patients (26%) exhibited collateral vessels to the ischemic areas. No correlation was found between the presence of RC and collateral circulation (P = 0.384), or between the depth of reciprocal ST-depression and the degree of the collateral circulation (P = 0.195). However, 84% of patients without collaterals exhibited resolution of RC after successful percutaneous coronary intervention (PCI) (P = 0.036), suggesting that the ST depressions that resolved after reperfusion were directly caused by the culprit vessel. Patients without RC presented late after symptom onset (9.25 versus 3.83 hours, P = 0.004), also suggesting time related resolution., Conclusions: RC had no relation to or predictive value for collaterals on angiography. Among late presenting patients, RC were less frequent. Thus, reciprocal ST-depression may represent subendocardial ischemia from the primary coronary event or simply an electrical phenomenon, rather than ischemia at distance from impaired collateral circulation., (Published by Elsevier Inc.)

The syndrome of heart failure involves complex pathophysiologic mechanisms and is associated with extremely high-morbidity, mortality and economic costs. This growing global epidemic has diverse etiologies and is fundamentally characterized by dyshomeostasis between heart and kidneys, leading to development and progression of the cardiorenal syndrome. Excessive and sustained sympathoexcitation has emerged as a single prominent factor involved in the structural and functional dysfunction of multiple organ systems during this disease. Studies in experimental models of heart failure indicate that ablation of the renal nerves may help restore renal sodium and water equilibrium as well as the attenuation of adverse cardiac remodeling. With the recent development of minimally invasive endovascular renal denervation in humans, it is anticipated that this technology would become a novel and important paradigm shift in the management of heart failure., (Copyright © 2017. Published by Elsevier Inc.)

Leptin is a 16-kDa peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake, elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. Although the relevance of endogenous leptin needs further clarification, it appears to function as a pressure- and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular and cardiac damage.

Cardiac troponins are the preferred biomarkers for the determination of acute myocardial necrosis. The high sensitivity of the available assays has significantly increased the detection of microscopic amounts of myocardial damage. Although compelling evidence indicates that elevated cardiac troponins are markers of poor prognosis and increased mortality, irrespective of the clinical scenario, small elevations can be seen in protean conditions and may confound the diagnosis of acute coronary syndromes. Emerging evidence suggests multiple different cellular mechanisms leading to cardiac troponin release, which challenge long held paradigms such as equivalency between troponin release into the circulation and irreversible cell death. Hence, knowledge of the physiology and pathophysiology of these cardiac biomarkers is essential for their accurate interpretation and consequent correct clinical diagnosis. Herein, the current relevant information about cardiac troponins is discussed, with special emphasis on pathophysiology and clinical correlates.

Heart failure constitutes a significant source of morbidity and mortality in the United States and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This complex interaction is characterized by a pathophysiological disequilibrium between the heart and the kidney, in which cardiac malfunction promotes renal impairment, which in turn feeds back for further deterioration of cardiovascular function. Multiple neurohumoral and hemodynamic mechanisms are involved in this cardiorenal dyshomeostasis, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with cardiorenal dysfunction can be challenging and should be individualized. Emerging therapies must address the impairment of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is warranted to achieve optimal results.

Heart failure constitutes a significant source of morbidity and mortality in the United States, and its incidence and prevalence continue to grow, increasing its burden on the healthcare system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phenomenon characterized by a pathophysiologic disequilibrium between the heart and the kidney, in which malfunction of 1 organ consequently promotes the impairment of the other. Multiple neurohumoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is recommended to achieve optimal results.

Takotsubo cardiomyopathy also known as transient ballooning syndrome is characterized by reversible left ventricular dysfunction with presentation mimicking myocardial infarction. Even though this syndrome has been recognized for nearly 2 decades, cases with atypical features are still being reported. We describe 2 patients who presented to the hospital after cardiac arrest, which is very rare according to previous reports. Although still considered a benign condition, transient ballooning syndrome could be responsible for some of the undiagnosed sudden cardiac deaths in the community, and it may have a worse prognosis than currently recognized. In addition, 1 of our patients also had a previously unreported triggering factor, namely sexual intercourse.

Neurally-mediated syncope is the most common cause of transient loss of consciousness. In this report, we describe an index case of a 43-year-old man with multiple episodes of neurally-mediated syncope. He underwent tilt-table testing, resulting in asystole for 15 seconds with generalized convulsions. After permanent pacemaker implantation, the patient had another syncopal episode requiring adjustment of pacemaker settings. Current concepts of the pathophysiology as well as the diagnosis and management of this condition are discussed.

The incidence and prevalence of obesity has risen markedly in the last decade, and this epidemic represents a serious health hazard with significant morbidity and mortality. Although hypertension is recognized as one of the most serious consequences of obesity, its pathophysiology remains incompletely understood. Contemporary research suggests that the recently discovered hormone leptin may represent a common link between these 2 pathologic conditions. Leptin is primarily synthesized and secreted by adipocytes. One of the major functions of this hormone is the control of energy balance. By binding to receptors in the hypothalamus, it reduces food intake and promotes elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect actions, may play an important role in cardiovascular and renal functions. Although the relevance of endogenous leptin needs further clarification for the control of renal sodium excretion and vascular tone, it appears to be a potential pressure and volume-regulating factor in normal situations. However, in conditions of chronic hyperleptinemia, such as obesity, leptin may function pathophysiologically for the development of hypertension as well as cardiac and renal disease. Thus, in addition to weight control, reduction of circulating leptin may confer cardiovascular and renal protective effects in patients with obesity-hypertension.

The metabolic syndrome is most commonly defined as the presence of three or more of the following atherogenic risk factors: increased abdominal waist circumference, hypertriglyceridemia, low serum high-density lipoprotein level, raised blood pressure, and a fasting blood sugar level greater than 110 mg/dL. It is associated with increased risk for the development of atherosclerosis and cardiovascular disease. Current management recommendations promote therapeutic lifestyle changes (mainly diet and exercise) for all of the core elements of the syndrome. Pharmacologic therapy is indicated in most patients with atherogenic dyslipidemia and in some with hyperglycemia and raised blood pressure. These therapeutic measures are able to favorably modify the core components of the metabolic syndrome and it is hoped that they will also improve the long-term cardiovascular prognosis in patients with this disorder.

Background: Earlier studies have indicated that the atrial natriuretic factor prohormone fragment 31-67 (Pro ANF31-67) has important effects for the promotion of sodium excretion and vasodilation in several animal species. However, the mechanisms for the natriuretic actions of Pro ANF31-67 are not completely defined. In the present study, the effects of synthetic Pro ANF31-67 on renin secretion were examined in sodium-depleted, anesthetized dogs with a single intact kidney (n = 5)., Methods: After 3 20-minute control renal clearance periods, synthetic dog Pro ANF31-67 was given intrarenally at a sustained dose of 0.03 microg/kg/min for 3 20-minute experimental intervals, and after discontinuation of the peptide infusion, 3 final 20-minute recovery periods were determined., Results: Sustained intrarenal infusions of the Pro ANF31-67 produced striking decrements (p<0.05) in renin secretion, from a control value of 1418 +/- 243 to 401 +/- 223 ng of angiotensin I/min. This 66% fall in renin secretion was associated with significant (P < 0.05) increases in creatinine clearance (40%), renal blood flow (8%), urine flow (50%), and sodium excretion (17%)., Conclusions: It is suggested that this inhibition of renin secretion was mediated, at least in part, in response to a ProANF31-67-induced increment in the sodium load delivered to the macula densa. An interaction of the peptide with the renal vascular receptor for suppression of renin release is also possible. ProANF31-67 may represent an important hormonal mechanism involved in the regulation of body-fluid balance.

The interaction between renal prostaglandins and atrial natriuretic factor (ANF) for the regulation of renal hemodynamic and excretory function was examined in conscious dogs with arteriovenous fistula and chronic compensated high-output heart failure (n = 6). After two control clearance periods, 100 ng/kg/min ANF was administered for the duration of the study. After two clearance periods with ANF infusions, 10 mg/kg indomethacin intravenous bolus was given, and three additional clearance periods were obtained. Atrial natriuretic factor alone increased sodium excretion from a baseline of 25 +/- 7 microEq/min to 158 +/- 24 microEq/min (P < 0.05), whereas creatinine clearance was elevated by 9 mL/min (P < 0.05). Indomethacin reduced ANF-induced sodium excretion and creatinine clearance by 75% (P < 0.05) and 35% (P < 0.05), respectively. In a time control series in dogs with arteriovenous fistula (n = 4), indomethacin vehicle did not alter ANF-induced natriuresis or renal hemodynamic function. These results suggest a modulatory role of the prostaglandins on the renal response to ANF infusions in this canine model of compensated heart failure.