Peter A. McCullough M.D.

Afzal, A., R. C. Vallabhan and P. A. McCullough (2017). “Acute kidney injury in cardiogenic shock: In search of early detection and clinical certainty.” Eur J Heart Fail: 1-3.

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This study stands out as the rst study to prospectively eval-uate AKI in patients with CS by KDIGO guidelines, based notonly on creatinine, but also on cystatin C.5The AKI mortal-ity results in this study are internally consistent as patients pre-senting with A KI had lower ejection fractions, higher Sequen-tial Organ Failure Assessment scores, and a higher incidenceof respiratory failure requiring mechanical ventilation.7Rates ofrenal replacement therapy were 14%, yet the 90-day mortalityrate was 38% suggesting that the majority of deaths in the rst20 days reected the natural history of CS treated with stan-dard of care in the cardiac catheterization laboratory and coro-nary care unit and were not amenable to ultraltration for pul-monary oedema/anuria or haemodialtration for hyperkalaemia orazotaemia.

Kovesdy, C. P., L. J. Appel, M. E. Grams, L. Gutekunst, P. A. McCullough, B. F. Palmer, B. Pitt, D. A. Sica and R. R. Townsend (2017). “Potassium homeostasis in health and disease: A scientific workshop cosponsored by the national kidney foundation and the american society of hypertension.” J Am Soc Hypertens: 2017 Oct [Epub ahead of print].

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While much emphasis, and some controversy, centers on recommendations for sodium intake, there has been considerably less interest in recommendations for dietary potassium intake, in both the general population and patients with medical conditions, particularly acute and chronic kidney disease. Physiology literature and cohort studies have noted that the relative balance in sodium and potassium intakes is an important determinant of many of the sodium-related outcomes. A noteworthy characteristic of potassium in clinical medicine is the extreme concern shared by many practitioners when confronted by a patient with hyperkalemia. Fear of this often asymptomatic finding limits enthusiasm for recommending potassium intake and often limits the use of renin-angiotensin-aldosterone system blockers in patients with heart failure and chronic kidney diseases. New agents for managing hyperkalemia may alter the long-term management of heart failure and the hypertension, proteinuria, and further function loss in chronic kidney diseases. In this jointly sponsored effort between the American Society of Hypertension and the National Kidney Foundation, 3 panels of researchers and practitioners from various disciplines discussed and summarized current understanding of the role of potassium in health and disease, focusing on cardiovascular, nutritional, and kidney considerations associated with both hypo- and hyperkalemia.

Palazzuoli, A., G. Ruocco, O. De Vivo, R. Nuti and P. A. McCullough (2017). “Prevalence of hyperuricemia in patients with acute heart failure with either reduced or preserved ejection fraction.” Am J Cardiol 120(7): 1146-1150.

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The relation between uric acid (UA) and heart failure has been described; however, there is little detail concerning acute heart failure (AHF) in patients with reduced versus preserved ejection fraction heart failure (HFrEF, HFpEF). We studied 324 consecutive AHF patients screened from interventional Diur-HF Trial (NCT01441245) from January 2011 to February 2016, and divided into HFrEF (EF <50%) and HFpEF (EF >/=50%). We defined hyperuricemia as serum UA >/=7.0 mg/dL in men and >/=6 mg/dL in women. Patients were followed up for 6 months after discharge. The primary outcome was heart failure hospitalization or death. Among 173 HFrEF and 151 HFpEF cases, hyperuricemia was found in 43% and 57%, respectively (p = 0.01). Hyperuricemia was also more frequent in women (74% vs 60%; p = 0.008), those with diabetes (39% vs 19%; p <0.001), hypertension (62% vs 43%; p = 0.001), and atrial fibrillation (48% vs 34%; p = 0.01). In patients with HFrEF, univariate analysis found that hyperuricemia (hazard ratio [HR] 1.48, 95% confidence interval [CI] 1.02 to 2.15; p = 0.04) and congestion score >/=3 (HR 2.83, 95% CI 1.52 to 5.28; p <0.001) were associated with the primary end point; after adjustment, only congestion score >/=3 (HR 2.08, 95% CI 1.06 to 4.10; p = 0.03) confirmed this trend. Conversely, in patients with HFpEF, hyperuricemia was the only significant predictor of the primary end point both in univariate (HR 2.25, 95% CI 1.44 to 3.50; p <0.001) and multivariate analyses (HR 2.38, 95% CI 1.32 to 4.28; p = 0.004). In conclusion, in AHF hyperuricemia is common in both in HFrEF and in HFpEF. In the HFpEF subgroup, hyperuricemia was the only independent predictor of heart failure hospitalization or death.

Azzalini, L., L. Candilio, P. A. McCullough and A. Colombo (2017). “Current risk of contrast-induced acute kidney injury after coronary angiography and intervention: A reappraisal of the literature.” Can J Cardiol 33(10): 1225-1228.

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Contrast-induced acute kidney injury (CI-AKI) is the acute impairment of renal function further to the intravascular administration of iodinated contrast media, and occurs most frequently after coronary angiography, percutaneous coronary intervention, and contrast-enhanced computed tomography. CI-AKI has been associated with the development of acute renal failure, worsening of chronic kidney disease, requirement for dialysis, prolonged hospital stay, and higher mortality rates and health care costs. Recently, a number of studies suggested that contrast media exposure might not be the causative agent in the occurrence of acute kidney injury, particularly in stable patients who receive small to moderate amounts of contrast media. However, those who undergo coronary angiography and intervention are indeed subject to an increased hazard of CI-AKI, in view of a more significant contrast media exposure as well as the presence of concomitant risk factors. Solid randomized clinical trials are therefore required to identify preventative strategies to reduce the risk of CI-AKI and its complications in these patients.

Butler, J., C. E. Hamo, G. Filippatos, S. J. Pocock, R. A. Bernstein, M. Brueckmann, A. K. Cheung, J. T. George, J. B. Green, J. L. Januzzi, S. Kaul, C. S. P. Lam, G. Y. H. Lip, N. Marx, P. A. McCullough, C. R. Mehta, P. Ponikowski, J. Rosenstock, N. Sattar, A. Salsali, B. M. Scirica, S. J. Shah, H. Tsutsui, S. Verma, C. Wanner, H. J. Woerle, F. Zannad and S. D. Anker (2017). “The potential role and rationale for treatment of heart failure with sodium-glucose co-transporter 2 inhibitors.” Eur J Heart Fail: 2017 Aug [Epub ahead of print].

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Heart failure (HF) and type 2 diabetes mellitus (T2DM) are both growing public health concerns contributing to major medical and economic burdens to society. T2DM increases the risk of HF, frequently occurs concomitantly with HF, and worsens the prognosis of HF. Several anti-hyperglycaemic medications have been associated with a concern for worse HF outcomes. More recently, the results of the EMPA-REG OUTCOME trial showed that the sodium-glucose co-transporter 2 (SGLT2) inhibitor empagliflozin was associated with a pronounced and precocious 32% reduction in cardiovascular mortality in subjects with T2DM and established cardiovascular disease. These benefits were more related to a reduction in incident HF events rather than to ischaemic vascular endpoints. Several mechanisms have been put forward to explain these benefits, which also raise the possibility of using these drugs as therapies not only in the prevention of HF, but also for the treatment of patients with established HF regardless of the presence or absence of diabetes. Several large trials are currently exploring this postulate.