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Hyperkalemia in ambulant postcardiac surgery patients during combined therapy with angiotensin-converting enzyme inhibitor, spironolactone, and diet rich in potassium: A report of two cases and review of literature.
Dixit, A, Majumdar, G, Tewari, P
Annals of cardiac anaesthesia. 2019;(2):162-168
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Abstract
INTRODUCTION Potassium is the most abundant cation in intracellular compartment. A deficiency or excess of its serum concentration can be deleterious to the one suffering from a cardiac ailment. Post cardiac surgery patients are often on multiple drugs like angiotensin receptor blockers (ARBs), angiotensin converting enzyme inhibitors (ACEI), diuretics including potassium sparing diuretics which are known to predispose for hyperkalemia. We report two postoperative cases who developed life threatening hyperkalemia despite normal renal function due to a combination of factors like treatment with ACEI, potassium sparing diuretics, high dietary intake of potassium and we also discuss renal handling of potassium in this review of literature. METHODOLOGY We present a case series of two cases of cardiac surgery, who presented in the emergency department with hyperkalemia, managed conservatively and detailed history revealed that patient were also on very high nutritional potassium. RESULT Both the patients responded to conservative management and there was no recurrence of such episodes once the dose of diuretics was adjusted and diet modification advised. CONCLUSION In India, many patients are from a low socioeconomic background and often resort to cheap and filling food items like bananas. This dietary factor should be kept in mind while prescribing patients with these medications and adequate counseling regarding diet should be done.
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Heart Failure Update: Outpatient Management.
Wojnowich, K, Korabathina, R
FP essentials. 2016;:18-25
Abstract
Outpatient management of heart failure (HF) is aimed at treating symptoms and preventing hospitalizations and readmissions. Management is initiated in a stepwise approach. Blockade of the renin-angiotensin system is a cornerstone of therapy and should be started, along with beta blockers, as soon as the diagnosis of HF is made. Other drugs, including diuretics, aldosterone antagonists, hydralazine, and nitrates, may be added based on symptoms and American College of Cardiology/American Heart Association stage. Despite a great interest in and theoretical benefit of naturoceutical products in the mitigation of oxidative stress and HF progression, none has been proven to be beneficial, and concerns exist regarding their interactions with standard HF drugs. Other nonpharmacologic interventions, including sodium restriction, regular exercise, and/or cardiac rehabilitation, should be initiated at diagnosis. HF often is progressive, and clinicians should be aware of late stage management options, including implantable devices, cardiac transplantation, and hospice care.
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Management of hypertension and heart failure in patients with Addison's disease.
Inder, WJ, Meyer, C, Hunt, PJ
Clinical endocrinology. 2015;(6):789-92
Abstract
Addison's disease may be complicated by hypertension and less commonly by heart failure. We review the pathophysiology of the renin-angiotensin-aldosterone axis in Addison's disease and how this is altered in the setting of hypertension and heart failure. An essential first step in management in both conditions is optimizing glucocorticoid replacement and considering dose reduction if excessive. Following this, if a patient with Addison's disease remains hypertensive, the fludrocortisone dose should be reviewed and reduced if there are clinical and/or biochemical signs of mineralocorticoid excess. In the absence of such signs, where the renin is towards the upper end of the normal range or elevated, an angiotensin II (AII) receptor antagonist or angiotensin converting enzyme (ACE) inhibitor is the treatment of choice, and the fludrocortisone dose should remain unchanged. Dihydropyridine calcium channel blockers are clinically useful as second line agents, but diuretics should be avoided. In the setting of heart failure, there is an increase in total body sodium and water; therefore, it is appropriate to reduce and rarely consider ceasing the fludrocortisone. Loop diuretics may be used, but not aldosterone antagonists such as spironolactone or eplerenone. Standard treatment with ACE inhibitors, or as an alternative, AII receptor antagonists, are appropriate. Measurements of renin are no longer helpful in heart failure to determine the volume status but plasma levels of brain natriuretic peptide (BNP/proBNP) may help guide therapy.
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Combined treatment of vitamin K2 and angiotensin-converting enzyme inhibitor ameliorates hepatic dysplastic nodule in a patient with liver cirrhosis.
Yoshiji, H, Noguchi, R, Yamazaki, M, Ikenaka, Y, Sawai, M, Ishikawa, M, Kawaratani, H, Mashitani, T, Kitade, M, Kaji, K, et al
World journal of gastroenterology. 2007;(23):3259-61
Abstract
Although it is well known that the hepatocellular carcinoma (HCC) is an ominous complication in patients with liver cirrhosis, there has been no approved drug to prevent the development of HCC to date. We previously reported that the combined treatment of vitamin K2 (VK) and angiotensin-converting enzyme inhibitor (ACE-I) significantly suppressed the experimental hepatocarcinogenesis. A 66-year-old Japanese woman with hepatitis C virus (HCV)-related liver cirrhosis developed a dysplastic nodule in the liver detected by enhanced computed tomography along with elevation of the tumor markers, namely, alpha-fetoprotein (AFP) and lectin-reactive demarcation (AFP-L3), suggesting the presence of latent HCC. After oral administration of VK and ACE-I, the serum levels of both AFP and AFP-L3 gradually decreased without any marked alteration of the serum aminotransferase activity. After one-year treatment, not only the serum levels of AFP and AFP-L3 returned to the normal ranges, but also the dysplastic nodule disappeared. Since both VK and ACE-I are widely used without serious side effects, this combined regimen may become a new strategy for chemoprevention against HCC.
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Iron supplementation inhibits cough associated with ACE inhibitors.
Lee, SC, Park, SW, Kim, DK, Lee, SH, Hong, KP
Hypertension (Dallas, Tex. : 1979). 2001;(2):166-70
Abstract
Dry cough is the most common limiting factor of ACE inhibitor (ACEI) use. Generation of NO, a proinflammatory substance on bronchial epithelial cells, is increased by ACEI. Using a randomized, double-blind, placebo-controlled trial, we tested the hypothesis that supplementing iron, an inhibitor of NO synthase, may reduce the cough associated with ACEI use. The subjects were 19 patients who had developed ACEI-induced cough. After a 2-week observation period, they were randomized to a daily morning dose of either 256-mg ferrous sulfate as a tablet or placebo for a treatment period of 4 weeks. The subjects were requested to fill out a cough diary by scoring the daily severity of the cough on a scale of 0 to 4. Mean daily cough scores for the last week of the observation and treatment period were compared. Changes in blood cell count and serum iron and ferritin concentration between the 2 periods were evaluated. Mean daily cough scores during the observation and treatment periods were 3.07+/-0.70 and 1.69+/-1.10, respectively, for the iron group and 2.57+/-0.80 and 2.35+/-1.22, respectively, for the placebo group, showing a significant reduction in cough scores with iron supplementation (P<0.01) but not with placebo. Three subjects in the iron group showed almost complete cough abolition. No significant changes in laboratory data were observed in either group. In conclusion, iron supplementation successfully decreases ACEI-induced cough. This effect may be related to the decrease of NO generation associated with the inhibition of NO synthase activity in bronchial epithelial cells.