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Tomas Jernberg - One of the best experts on this subject based on the ideXlab platform.
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randomized evaluation of Beta Blocker and ace inhibitor angiotensin receptor Blocker treatment in patients with myocardial infarction with non obstructive coronary arteries minoca bat rationale and design
American Heart Journal, 2021Co-Authors: Anna M Nordenskjold, Stefan Agewall, Dan Atar, Tomasz Baron, John F Beltrame, Olle Bergstrom, David Erlinge, Chris P Gale, Javier Lopezpais, Tomas JernbergAbstract:Myocardial infarction with non-obstructive coronary arteries (MINOCA) is common and occurs in 6-8% of all patients fulfilling the diagnostic criteria for acute myocardial infarction (AMI). This paper describes the rationale behind the trial 'Randomized Evaluation of Beta Blocker and ACE-Inhibitor/Angiotensin Receptor Blocker Treatment (ACEI/ARB) of MINOCA patients' (MINOCA-BAT) and the need to improve the secondary preventive treatment of MINOCA patients. METHODS: MINOCA-BAT is a registry-based, randomized, parallel, open-label, multicenter trial with 2:2 factorial design. The primary aim is to determine whether oral Beta blockade compared with no oral Beta blockade, and ACEI/ARB compared with no ACEI/ARB, reduce the composite endpoint of death of any cause, readmission because of AMI, ischemic stroke or heart failure in patients discharged after MINOCA without clinical signs of heart failure and with left ventricular ejection fraction ≥40%. A total of 3500 patients will be randomized into four groups; e.g. ACEI/ARB and Beta Blocker, Beta Blocker only, ACEI/ARB only and neither ACEI/ARB nor Beta Blocker, and followed for a mean of 4 years. SUMMARY: While patients with MINOCA have an increased risk of serious cardiovascular events and death, whether conventional secondary preventive therapies are beneficial has not been assessed in randomized trials. There is a limited basis for guideline recommendations in MINOCA. Furthermore, studies of routine clinical practice suggest that use of secondary prevention therapies in MINOCA varies considerably. Thus results from this trial may influence future treatment strategies and guidelines specific to MINOCA patients.
Cathleen Clancy - One of the best experts on this subject based on the ideXlab platform.
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characterization of fatal Beta Blocker ingestion a review of the american association of poison control centers data from 1985 to 1995
Clinical Toxicology, 1997Co-Authors: Jeffrey N Love, Toby L Litovitz, John M Howell, Cathleen ClancyAbstract:OBJECTIVE: To characterize Beta Blocker-related deaths. METHODS: This is a retrospective review of Beta Blocker-related exposure data and fatality case abstracts reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System during the 11 year period, 1985 to 1995. Historical and laboratory data were used to determine those fatalities which resulted primarily from Beta Blocker intoxication. RESULTS: Of 52,156 reported Beta Blocker exposures, 164 were fatal. In 38 cases, Beta Blockers were implicated as the primary cause of death. Propranolol was responsible for the greatest number of exposures (44%) and implicated as the cause of death in a disproportionately high percentage of fatalities (71%). Patients were generally young women; 63% were female and 92% were less than 50 years old. The dysrhythmias most often noted in fatal cases were bradycardia and asystole. Cardiopulmonary arrest did not develop until patients were in the care of health care personnel in 59% of cases. Though glucagon was initiated more often than any other intervention in fatal intoxications (83%), optimal dosing and maintenance infusions appear to have been underutilized. CONCLUSIONS: The predominance of fatalities associated with propranolol compared to other Beta Blockers reflects both its greater frequency of use over the time period studied and its greater toxicity. Since 59% developed. cardiac arrest after reaching health care personnel, further study should focus on identifying medical intervention that can reduce mortality in this group.
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characterization of fatal Beta Blocker ingestion a review of the american association of poison control centers data from 1985 to 1995
Clinical Toxicology, 1997Co-Authors: Jeffrey N Love, Toby L Litovitz, John M Howell, Cathleen ClancyAbstract:AbstractObjective: To characterize Beta Blocker-related deaths. Methods: This is a retrospective review of Beta Blocker-related exposure data and fatality case abstracts reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System during the 11 year period, 1985 to 1995. Historical and laboratory data were used to determine those fatalities which resulted primarily from Beta Blocker intoxication. Results: Of 52,156 reported Beta Blocker exposures, 164 were fatal. In 38 cases, Beta Blockers were implicated as the primary cause of death. Propranolol was responsible for the greatest number of exposures (44%) and implicated as the cause of death in a disproportionately high percentage of fatalities (71%). Patients were generally young women; 63% were female and 92% were less than 50 years old. The dysrhythmias most often noted in fatal cases were bradycardia and asystole. Cardiopulmonary arrest did not develop until patients were in the care of health care personnel in 59%...
Anna M Nordenskjold - One of the best experts on this subject based on the ideXlab platform.
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randomized evaluation of Beta Blocker and ace inhibitor angiotensin receptor Blocker treatment in patients with myocardial infarction with non obstructive coronary arteries minoca bat rationale and design
American Heart Journal, 2021Co-Authors: Anna M Nordenskjold, Stefan Agewall, Dan Atar, Tomasz Baron, John F Beltrame, Olle Bergstrom, David Erlinge, Chris P Gale, Javier Lopezpais, Tomas JernbergAbstract:Myocardial infarction with non-obstructive coronary arteries (MINOCA) is common and occurs in 6-8% of all patients fulfilling the diagnostic criteria for acute myocardial infarction (AMI). This paper describes the rationale behind the trial 'Randomized Evaluation of Beta Blocker and ACE-Inhibitor/Angiotensin Receptor Blocker Treatment (ACEI/ARB) of MINOCA patients' (MINOCA-BAT) and the need to improve the secondary preventive treatment of MINOCA patients. METHODS: MINOCA-BAT is a registry-based, randomized, parallel, open-label, multicenter trial with 2:2 factorial design. The primary aim is to determine whether oral Beta blockade compared with no oral Beta blockade, and ACEI/ARB compared with no ACEI/ARB, reduce the composite endpoint of death of any cause, readmission because of AMI, ischemic stroke or heart failure in patients discharged after MINOCA without clinical signs of heart failure and with left ventricular ejection fraction ≥40%. A total of 3500 patients will be randomized into four groups; e.g. ACEI/ARB and Beta Blocker, Beta Blocker only, ACEI/ARB only and neither ACEI/ARB nor Beta Blocker, and followed for a mean of 4 years. SUMMARY: While patients with MINOCA have an increased risk of serious cardiovascular events and death, whether conventional secondary preventive therapies are beneficial has not been assessed in randomized trials. There is a limited basis for guideline recommendations in MINOCA. Furthermore, studies of routine clinical practice suggest that use of secondary prevention therapies in MINOCA varies considerably. Thus results from this trial may influence future treatment strategies and guidelines specific to MINOCA patients.
Joel S Holger - One of the best experts on this subject based on the ideXlab platform.
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high dose insulin therapy in Beta Blocker and calcium channel Blocker poisoning
Clinical Toxicology, 2011Co-Authors: Kristin M Engebretsen, Kathleen M Kaczmarek, Jenifer Morgan, Joel S HolgerAbstract:Introduction. High-dose insulin therapy, along with glucose supplementation, has emerged as an effective treatment for severe BetaBlocker and calcium channel-Blocker poisoning. We review the experimental data and clinical experience that suggests high-dose insulin is superior to conventional therapies for these poisonings. Presentation and general management. Hypotension, bradycardia, decreased systemic vascular resistance (SVR), and cardiogenic shock are characteristic features of Beta-Blocker and calcium-channel Blocker poisoning. Initial treatment is primarily supportive and includes saline fluid resuscitation which is essential to correct vasodilation and low cardiac filling pressures. Conventional therapies such as atropine, glucagon and calcium often fail to improve hemodynamic status in severely poisoned patients. Catecholamines can increase blood pressure and heart rate, but they also increase SVR which may result in decreases in cardiac output and perfusion of vascular beds. The increased myocardial oxygen demand that results from catecholamines and vasopressors may be deleterious in the setting of hypotension and decreased coronary perfusion. Methods. The Medline, Embase, Toxnet, and Google Scholar databases were searched for the years 1975‐2010 using the terms: highdose insulin, hyperinsulinemia‐euglycemia, Beta-Blocker, calcium-channel Blocker, toxicology, poisoning, antidote, toxin-induced cardiovascular shock, and overdose. In addition, a manual search of the Abstracts of the North American Congress of Clinical Toxicology and the Congress of the European Association of Poisons Centres and Clinical Toxicologists published in Clinical Toxicology for the years 1996‐2010 was undertaken. These searches identified 485 articles of which 72 were considered relevant. Mechanisms of high-dose insulin benefit. There are three main mechanisms of benefit: increased inotropy, increased intracellular glucose transport, and vascular dilatation. Efficacy of high-dose insulin. Animal models have shown high-dose insulin to be superior to calcium salts, glucagon, epinephrine, and vasopressin in terms of survival. Currently, there are no published controlled clinical trials in humans, but a review of case reports and case series supports the use of high-dose insulin as an initial therapy. High-dose insulin treatment protocols. When first introduced, insulin doses were cautiously initiated at 0.5 U/kg bolus followed by a 0.5‐1 U/kg/h continuous infusion due to concern for hypoglycemia and electrolyte imbalances. With increasing clinical experience and the publication of animal studies, high-dose insulin dosing recommendations have been increased to 1 U/kg insulin bolus followed by a 1‐10 U/kg/h continuous infusion. Although the optimal regimen is still to be determined, bolus doses up to 10 U/kg and continuous infusions as high as 22 U/kg/h have been administered with good outcomes and minimal adverse events. Adverse effects of high-dose insulin. The major anticipated adverse events associated with high-dose insulin are hypoglycemia and hypokalemia. Glucose concentrations must be monitored regularly and supplementation of glucose will likely be required throughout therapy and for up to 24 h after discontinuation of high-dose insulin. The change in serum potassium concentrations reflects a shifting of potassium from the extracellular to intracellular space rather than a decrease in total body stores. Conclusions. While more clinical data are needed, animal studies and human case reports demonstrate that high-dose insulin (1‐10 U/kg/ hour) is a superior treatment in terms of safety and survival in both Beta-Blocker and calcium-channel Blocker poisoning. High-dose insulin should be considered initial therapy in these poisonings.
John J V Mcmurray - One of the best experts on this subject based on the ideXlab platform.
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efficacy and tolerability of adding an angiotensin receptor Blocker in patients with heart failure already receiving an angiotensin converting inhibitor plus aldosterone antagonist with or without a Beta Blocker findings from the candesartan in heart
European Journal of Heart Failure, 2008Co-Authors: R A P Weir, John J V Mcmurray, Margareta Puu, Scott D Solomon, Bertil Olofsson, Christopher B Granger, Salim Yusuf, Eric L MichelsonAbstract:Background: The efficacy and safety of adding an angiotensin receptor Blocker (ARB) in heart failure (HF) patients already taking an angiotensin-converting enzyme-inhibitor (ACE-I) plus an aldosterone antagonist is uncertain (especially if taking a Beta Blocker as well). The CHARM-Added trial describes the largest experience of using multiple inhibitors of the renin–angiotensin–aldosterone system (RAAS) together. Methods and results: 2548 HF patients, taking an ACE-I (936 no spironolactone/no Beta Blocker; 1175 no spironolactone/Beta Blocker; 199 spironolactone/no Beta Blocker; 238 sprionolactone/Beta Blocker), were randomized to placebo or candesartan and followed for 41 months (median). The primary outcome was cardiovascular death or HF hospitalization. In patients taking both a Beta Blocker and spironolactone (in addition to an ACE-I) at baseline, the candesartan:placebo hazard ratio was 0.85(95% CI 0.56, 1.29), compared to 0.85(95% CI 0.75, 0.96) in all randomized patients (interaction p value 0.49). The relative risk of discontinuation of candesartan (compared to placebo) because of hypotension, increased serum creatinine or hyperkalemia was not increased in patients taking spironolactone at baseline. Conclusions: An ARB may provide added benefit, at acceptable risk, in HF patients already taking spironolactone as well as an ACE-I and Beta Blocker. These findings must be confirmed in a prospective randomized trial before this approach can be recommended, routinely.
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effects of aldosterone receptor blockade in patients with mild moderate heart failure taking a Beta Blocker
European Journal of Heart Failure, 2007Co-Authors: Colin Berry, N F Murphy, Giuseppe De Vito, Stuart D R Galloway, Alison Seed, Carol Fisher, Naveed Sattar, P Vallance, Sewart W Hillis, John J V McmurrayAbstract:Aims: Spironolactone improves prognosis in severe heart failure (HF). We investigated its effects in patients with mild–moderate HF treated with an ACE inhibitor and Beta-Blocker. Randomised, double-blind, parallel-group, 3-month comparison of placebo and spironolactone (25 mg daily) in 40 patients in New York Heart Association (NYHA) class I (20%), II (70%) or III (10%), with a left ventricular ejection fraction of <40%. The mean (standard error) changes from baseline in the spironolactone and placebo groups were, respectively: i) B-type natriuretic peptide (BNP) −53.4(22.2) pg/mL and +3.3(12.1) pg/mL, P=0.04, ii) pro-collagen type III N-terminal amino peptide (PIIINP) −0.6(0.2) μmol/L and +0.02(0.2) μmol/L, P=0.02 and iii) creatinine +10.7(3.2) μmol/L and −0.3(2.6) μmol/L, P=0.01. Compared with placebo, spironolactone therapy was associated with a reduction in self-reported health-related quality of life: change in visual analog score: −6 (3) vs. +6 (4); P=0.01. No differences were observed on other biochemical, neurohumoral, exercise and autonomic function assessments. In patients with mild–moderate HF, spironolactone reduced neurohumoral activation (BNP) and a marker of collagen turnover (PIIINP) but impaired renal function and quality of life. The benefit–risk ratio of aldosterone blockade in mild HF is uncertain and requires clarification in a large randomised trial.