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1.
Prescribe an SGLT2 inhibitor for heart failure in the absence of diabetes?
Koenigsberger, D, Marquez, A, Hughes, PR
The Journal of family practice. 2021;(6):E7-E9
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Abstract
An RCT demonstrates that dapagliflozin produces better cardiovascular outcomes than placebo for heart failure patients with and without diabetes.
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2.
Using more frequent haemodialysis to manage volume overload in dialysis patients with heart failure, obesity or pregnancy.
Sangala, N, Ficheux, M, Fessi, H, Borman, N, Collins, A
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. 2020;(Suppl 2):ii11-ii17
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Abstract
Managing dialysis in patients with heart failure, pregnancy or obesity is complex. More frequent haemodialysis 5-6 days/week in randomized clinical trials has shown benefits for controlling volume overload, blood pressure and phosphorus, reducing left ventricular hypertrophy (LVH), and improving patient tolerance to therapy. Therapy prescriptions were guided by volume of urea cleared, time-integrated fluid loading control and increased phosphate-β2 microglobulin removal, with greater treatment frequency to address clinical efficacy targets. Case studies in all three categories show that treatment with more frequent haemodialysis in low-dialysate flow systems (Qd <200 mL/min, dialysate of 25-30 L/session, 5-7 days/week for 2.5-3.0 h/session) improves control of heart failure. In pregnancy, treatment 7 days/week with 30 L and 3 h/session of dialysis enabled successful delivery of infants at 32-34 weeks, with all doing well 2-5 years after birth. Obese patients with a body mass index (BMI) >35 achieved control of volume, blood pressure and uraemic symptoms compared to their prior 3 times/week in-centre haemodialysis. Greater application of more frequent haemodialysis should be considered, particularly in high-risk populations, to improve clinical care.
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3.
Adrenal pheochromocytoma presenting with Takotsubo-pattern cardiomyopathy and acute heart failure: A case report and literature review.
Chiang, YL, Chen, PC, Lee, CC, Chua, SK
Medicine. 2016;(36):e4846
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Abstract
BACKGROUND Pheochromocytoma is an endocrine tumor that causes hypertension, facial pallor, and headache. Pheochromocytoma patients rarely present with acute heart failure or cardiogenic shock. METHOD We discuss the case of a female patient with Takotsubo-pattern cardiomyopathy who presented with acute heart failure caused by pheochromocytoma. RESULT Treatment was adjusted based on the data of the pulse contour cardiac output system. After intensive hydration and medication for heart failure, the condition of the patient stabilized. CONCLUSION Before confirming the diagnosis, pulse contour cardiac output data could provide a direction for diagnosis and treatment.
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4.
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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The glucocorticoid in acute decompensated heart failure: Dr Jekyll or Mr Hyde?
Massari, F, Mastropasqua, F, Iacoviello, M, Nuzzolese, V, Torres, D, Parrinello, G
The American journal of emergency medicine. 2012;(3):517.e5-10
Abstract
Glucocorticoid administration is not recommended in patients with heart failure because of its related sodium and fluid retention. However, previous experimental and clinical studies have demonstrated that glucocorticoids can also induce a diuretic effect and improve renal function in patients with acute decompensated heart failure (ADHF) with refractory diuretic resistance. We report the case of a 65-year-old man with a known diagnosis of aortic stenosis, systolic ventricular dysfunction, and chronic obstructive pulmonary disease who was admitted for ADHF. After 3 days, during which resistance to conventional therapy was observed, intravenous methylprednisolone (60 mg/d) was added to ongoing medical treatment. Three days after the onset of glucocorticoid therapy, daily urine volume progressively increased (up to 5.8 L/d). Concurrently, signs and symptoms of congestion improved, the weight and brain natriuretic peptide plasma levels decreased (−7 kg and −46%, respectively) and glomerular filtration rate increased (+26%). Bioimpedance vector analysis showed a net reduction of fluid content (from 88.4% to 73.6% of hydration at discharge). In conclusion, this case report suggests that in a patient with ADHF and congestion resistant to diuretic therapy, glucocorticoid administration is safe and associated with improvement in congestion, neurohormonal status, and renal function. These data support the possible usefulness of glucocorticoids in this setting.
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Diuretic therapy in fluid-overloaded and heart failure patients.
Bellomo, R, Prowle, JR, Echeverri, JE
Contributions to nephrology. 2010;:153-163
Abstract
Diuretics are the most commonly used drugs to treat clinically diagnosed fluid overload in patients with heart failure. There is no conclusive evidence that they alter major outcomes such as survival to hospital discharge or time in hospital compared to other therapies. However, they demonstrably achieve fluid removal in the majority of patients, restore dry body weight, improve the breathlessness of pulmonary edema and are unlikely to be subjected to a large double-blind randomized controlled trial in this setting because of lack of equipoise. The effective and safe use of diuretics requires physiological understanding of the pharmacokinetics and pharmacodynamics of diuretic therapy, an appreciation of the clinical goals of diuretic therapy, the application of physiological targeting of dose, an understanding of the effects of hemodynamic impairment on their ability to achieve fluid removal, an appreciation of the effects of combinations of different diuretics in patients refractory to single agents and an understanding of the most common side effects of such therapy. The use of continuous infusions of loop diuretics, sometimes combined with carbonic anhydrase inhibitors and/or aldosterone antagonists and/or thiazide diuretics can prove particularly effective in patients with advanced heart failure. Such therapy often requires more intensive monitoring than available in medical wards. If diuretic therapy fails to achieve its clinical goals, ultrafiltration by semipermeable membranes is reliably effective in achieving targeted fluid removal. The combination of diuretic therapy and/or ultrafiltration can achieve volume control in essentially all patients with heart failure.
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7.
Supplemental ubiquinol in patients with advanced congestive heart failure.
Langsjoen, PH, Langsjoen, AM
BioFactors (Oxford, England). 2008;(1-4):119-28
Abstract
Patients with CHF, NYHA class IV, often fail to achieve adequate plasma CoQ10 levels on supplemental ubiquinone at dosages up to 900 mg/day. These patients often have plasma total CoQ10 levels of less than 2.5 microg/ml and have limited clinical improvement. It is postulated that the intestinal edema in these critically ill patients may impair CoQ10 absorption. We identified seven patients with advanced CHF (mean EF 22%) with sub-therapeutic plasma CoQ10 levels with mean level of 1.6 microg/ml on an average dose of 450 mg of ubiquinone daily (150-600 mg/day). All seven of these patients were changed to an average of 580 mg/day of ubiquinol (450-900 mg/day) with follow-up plasma CoQ10 levels, clinical status, and EF measurements by echocardiography. Mean plasma CoQ10 levels increased from 1.6 microg/ml (0.9-2.0 microg/ml) up to 6.5 microg/ml (2.6-9.3 microg/ml). Mean EF improved from 22% (10-35%) up to 39% (10-60%) and clinical improvement has been remarkable with NYHA class improving from a mean of IV to a mean of II (I to III). Ubiquinol has dramatically improved absorption in patients with severe heart failure and the improvement in plasma CoQ10 levels is correlated with both clinical improvement and improvement in measurement of left ventricular function.
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Heart failure with mitral valve regurgitation due to primary hyperoxaluria type 1: case report with review of the literature.
Van Driessche, L, Dhondt, A, De Sutter, J
Acta cardiologica. 2007;(2):202-6
Abstract
Primary hyperoxaluria type I (PH I) is a rare recessive autosomal disorder characterized by systemic calcium oxalate depositions, that results in renal failure and systemic oxalosis. We report a 38-year-old male with cardiac oxalosis, a severe complication of PHI, presenting with an infiltrative cardiomyopathy, secondary heart failure and severe mitral regurgitation, necessitating surgical repair to allow combined liver-kidney transplantation. We discuss pathogenesis, diagnostics and therapy of this clinical entity by reviewing literature.
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9.
[Continuous venovenous hemofiltration (CVVH) therapy in patient with refractory heart failure].
Matsumoto, K, Hayashi, T
Nihon rinsho. Japanese journal of clinical medicine. 2007;:255-8
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10.
Possible heart failure exacerbation associated with rosiglitazone: case report and literature review.
Page, RL, Gozansky, WS, Ruscin, JM
Pharmacotherapy. 2003;(7):945-54
Abstract
Increasing evidence suggests that neurohumoral manifestations of heart failure may lead to insulin resistance, predisposing patients with heart failure to the development of glucose intolerance or worsening of existing diabetes. Theoretically, insulin-sensitizing thiazolidinediones (TZDs) should be beneficial in this patient population. A 74-year-old man with well-compensated systolic dysfunction and longstanding type 2 diabetes mellitus treated with glyburide began therapy with rosiglitazone 4 mg/day, which was increased to 8 mg/day after 1 month. Two weeks later he was seen with a 5-kg weight gain, shortness of breath, bibasilar rales, +S3 gallop, and increased jugular venous distention. Twelve days later symptoms worsened, with pulmonary edema on chest radiograph, continued weight gain, and +4 pitting edema resistant to oral diuretics. The patient was admitted to the hospital for exacerbation of heart failure. Five days after discharge he was readmitted for similar symptoms, including an 11.8-kg weight gain. He reported adherence to drug therapy and diet. Rosiglitazone was immediately discontinued and 11 days later the man's weight stabilized to 79 kg and remained between 79 and 80 kg 2 and 3 months after discharge. This case demonstrates that TZDs may precipitate weight gain and pulmonary and peripheral edema in patients with stable heart failure. Earlier reports documented similar symptoms in patients without a history of heart failure. Although current recommendations state that TZDs should not be administered to patients with New York Heart Association class III or IV disease, practitioners should be aware that these adverse effects also may occur in patients with milder forms heart failure as well as those without heart failure.