scholarly journals Drug-Induced Heart Failure (Part 2: Mechanisms of Development, Clinical Signs, Differential Diagnosis, Risk Factors, Treatment and Prevention)

2020 ◽  
Vol 8 (2) ◽  
pp. 57-65
Author(s):  
O. D. Ostroumova ◽  
I. V. Goloborodova
Keyword(s):  
Heart Failure ◽  
Beta Blockers ◽  
Clinical Signs ◽  
Clinical Manifestations ◽  
Left Ventricular ◽  
Clinical Syndrome ◽  
Channel Blockers ◽  
Drug Induced ◽  
Treatment And Prevention ◽  
Developing Heart

Heart failure is a complex clinical syndrome caused by an impaired pumping function of the heart muscle, etiologically associated with cardiovascular disease and, in the vast majority of cases, requiring complex therapeutic regimens and simultaneous prescription of several drugs. To date, we know several classes of drugs (including those used for heart failure) which can induce development/progression of heart failure in both patients with left ventricular dysfunction, and in patients who do not have cardiovascular diseases. The aim of the study was to analyse and systematize data on development mechanisms, as well as methods of prevention and treatment of drug-induced heart failure when using diff erent groups of drugs. It has been established that drug-induced heart failure is most often associated with the use of calcium channel blockers (verapamil, diltiazem, nifedipine), beta-blockers, antiarrhythmic drugs (disopyramide, fl ecainide, propafenone, amiodarone, ibutilide, dofetilide, dronedarone), anthracyclines (doxorubicin) and other antitumor drugs (trastuzumab, bevacizumab, infl iximab), hypoglycemic drugs (thiazolidinediones, saxagliptin, alogliptin), and nonsteroidal anti-infl ammatory drugs, including selective cyclooxygenase-2 inhibitors. The study revealed various mechanisms of heart failure development following drug treatment. In some patients, heart failure development is associated with the cardiotoxic eff ect of a particular drug, in others with adverse eff ects on hemodynamics. Much depends on risks of developing heart failure, including specifi c risks attributable to groups of drugs and individual drugs. The identifi cation of drugs that can contribute to the development/ progression of heart failure, and possible clinical manifestations of drug-induced heart failure, as well as provision of timely information to physicians, and engagement of clinical pharmacologists with the aim of optimizing treatment of patients can facilitate timely diagnosis, treatment and prevention of drug-induced heart failure. 

scholarly journals Drug-Induced Heart Failure (Part 1: The Urgency of the Problem, the Prevalence, the Effect of Certain Groups of Drugs on the Risk of Development/Progression Heart Failure)

2020 ◽  
Vol 8 (1) ◽  
pp. 23-35
Author(s):  
O. D. Ostroumova ◽  
I. V. Goloborodova
Keyword(s):  
Heart Failure ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Beta Blockers ◽  
Modern Medicine ◽  
Left Ventricular ◽  
Medical Community ◽  
Channel Blockers ◽  
Drug Induced ◽  
Number Of Patients

Despite all the achievements of modern medicine, heart failure remains one of the most prevalent, severe and prognostically unfavorable conditions that requires close attention of the medical community. The diversity of the clinical picture and the large number of co-morbidities go hand in hand with a rather complicated pharmacotherapy regimen which, in the vast majority of cases, includes several medicines. Some classes of drugs can provoke the onset/progression of heart failure in patients with left ventricular dysfunction, as well as contribute to the development of heart failure in patients without concomitant cardiovascular diseases. The aim of the study was to analyse and systematise data on risk factors for the development of drug-induced heart failure and data on its prevalence when using various groups of medicines. It has been established that drug-induced heart failure typically develops in association with the use of calcium channel blockers (verapamil, diltiazem, nifedipine), beta-blockers (propranolol), antiarrhythmic drugs (disopyramide, dronedarone, lidocaine, lorcainide, mexiletine, moricizine, propafenone, tocainide, flecainide, encainide), hypoglycemic drugs (rosiglitazone, pioglitazone, saxagliptin), anthracyclines (doxorubicin, epirubicin) and other anticancer drugs (bevacizumab, infliximab, trastuzumab), and non-steroidal anti-infl ammatory drugs (diclofenac, ibuprofen, celecoxib, rofecoxib). It is assumed that this pathology develops in a small number of patients, mainly those who already have left ventricular dysfunction. However, the effects of drugs should be considered as one of potential and preventable causes of heart failure development/progression. Raising clinicians’ awareness of the potential adverse effects of individual medicines or entire pharmacological classes of drugs on the cardiac function, especially in patients with left ventricle dysfunction, can facilitate the timely diagnosis and prevention of drug-induced heart failure. 

scholarly journals The Management of Heart Failure with Preserved Ejection Fraction

2015 ◽  
Vol 1 (1) ◽  
pp. 11 ◽  
Author(s):  
Andrew JS Coats ◽  
Louise G Shewan ◽  
◽  
◽  
◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Beta Blockers ◽  
Angiotensin Receptor Blockers ◽  
Left Ventricular ◽  
Clinical Syndrome ◽  
Aldosterone Antagonists ◽  
Sharp Separation ◽  
Clinical Trial Evidence ◽  
Receptor Blockers

Heart failure is defined as a clinical syndrome and is known to present with a number of different pathophysiological patterns. There is a remarkable degree of variation in measures of left ventricular systolic emptying and this has been used to categorise heart failure into two separate types: low ejection fraction (EF) heart failure or HF-REF and high EF heart failure or HF-PEF. Here we review the pathophysiology, epidemiology and management of HF-PEF and argue that sharp separation of heart failure into two forms is misguided and illogical, and the present scarcity of clinical trial evidence for effective treatment for HF-PEF is a problem of our own making; we should never have excluded patients from major trials on the basis of EF in the first place. Whilst as many heart failure patients have preserved EFs as reduced we have dramatically under-represented HF-PEF patients in trials. Only four trials have been performed in HF-PEF specifically, and another two trials that recruited both HF-PEF and HF-REF can be considered. When we consider the similarity in outcomes and neurohormonal activation between HF-REF and HF-REF, the vast corpus of trial data that we have to attest to the efficacy of various treatment (angiotensinconverting-enzyme [ACE] inhibitors, angiotensin receptor blockers [ARBs], beta-blockers and aldosterone antagonists) in HF-REF, and the much more limited number of trials of similar agents showing near statistically significant benefits in HF-PEF the time has come rethink our management of HF-PEF, and in particular our selection of patients for trials.

The effect of oestrogen withdrawal on cardiac Ca2+ regulation and the influence of GPER1

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A.J Francis ◽  
J.M Firth ◽  
N Islam ◽  
J Gorelik ◽  
K.T MacLeod
Keyword(s):  
Heart Failure ◽  
Structural Integrity ◽  
Left Ventricular ◽  
Funding Source ◽  
Hormonal Changes ◽  
Ion Conductance ◽  
Developing Heart ◽  
Rapid Stimulation ◽  
Post Menopausal

Abstract Background Post-menopausal women have an enhanced risk of developing heart failure, attributed to declining oestrogen levels during menopause. However, the signalling mechanisms remain undetermined. Purpose We aim to determine the role of G-protein coupled oestrogenic receptor 1 (GPER1) in intracellular Ca2+ regulation and the consequences of hormonal changes that may exacerbate the pathophysiology of heart failure. Methods Ovariectomy (OVx) (mimics menopausal hormone changes) or sham surgeries were conducted on female guinea pigs. Left ventricular cardiomyocytes were isolated 150-days post-operatively for experimental use. Cellular t-tubule network and structural integrity was measured using fluorescent di-8-ANEPPs staining and scanning ion conductance microscopy. GPER1 expression and localisation was measured by Western blot and immunostaining. The role of GPER1 activation was measured using selective agonist G-1 in electrophysiological and Ca2+-sensitive dye fluorescence experiments. Results Following oestrogen withdrawal, the t-tubule network density decreased by 13% and z-groove index reduced by 15%. GPER1 predominantly localised to the peri-nuclear endoplasmic reticulum and its expression increased by 32% in OVx. Action potential duration (APD) prolonged in OVx and following GPER1 activation, APD90 shortened by 11% and 25% in sham and OVx respectively. OVx cells had larger peak inward Ca2+ current (ICaL) (by 22%) and sarcoplasmic reticulum (SR) Ca2+ content (by 13%), compared with sham. While GPER1 activation had little effect on peak ICaL or SR content, it reduced Ca2+ transient amplitude (by 20%), SR fractional release (by 11%) in OVx cells. The frequency of occurrence of spontaneous Ca2+ waves evoked by periods of rapid stimulation reduced by 40% and wave-free survival time prolonged in OVx cells following GPER1 activation. Conclusions In the hearts of an animal species whose electrophysiology and intracellular Ca2+ regulation is akin to humans, we show that following oestrogen deficiency, the t-tubule network is down-regulated and becomes disorganised, GPER1 expression is increased and its activation induces negative inotropic responses in cardiomyocytes. This may limit the adverse changes to Ca2+ signalling reported in OVx that could be pro-arrhythmic and exacerbate the progression to heart failure. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): British Heart Foundation

Abstract 13135: Starting Beta-blockers in Hypertension is Followed by Excess Loop Diuretic Use: Beta-blocker Induced Heart Failure?

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniel N Silverman ◽  
Jeanne d de Lavallaz ◽  
Timothy B Plante ◽  
Margaret M Infeld ◽  
Markus Meyer
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Beta Blocker ◽  
Antihypertensive Medication ◽  
Temporal Relationship ◽  
Loop Diuretic ◽  
Beta Blockers ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction

Introduction: Recent investigation has identified that discontinuation of beta-blockers in subjects with normal left ventricular ejection fraction (LVEF) leads to a reduction in natriuretic peptide levels. We investigated whether a similar trend would be seen in a hypertension clinical trial cohort. Methods: In 9,012 subjects hypertensive subjects without a history of symptomatic heart failure, known LVEF <35% or recent heart failure hospitalization enrolled in the Systolic Blood Pressure Intervention Trial (SPRINT), we compared incidence of loop diuretic initiation and time to initiation following start of a new anti-hypertensive medication. The categorical relationship (new antihypertensive class followed by loop-diuretic use) and temporal relationship (time to loop diuretic initiation) were each analyzed. The categorical relationship was assessed using a Pearson’s chi-squared test and the temporal relationship using a Wilcoxon rank sum test. Bonferroni-corrected p-values were utilized for all comparisons. Results: Among the 9,012 subjects analyzed, the incidence of anti-hypertensive initiation and loop diuretic initiation was greatest following start of a beta-blocker (16.6%) compared with other antihypertensive medication classes (calcium channel blocker 13.8%, angiotensin converting enzyme-inhibitor/angiotensin receptor blocker 12.9% and thiazide diuretic 10.2%; p<0.001). In addition, the median time between starting a new antihypertensive medication and loop diuretic was the shortest for beta-blockers and longest for thiazides (both p <0.01). No significant differences in renal function were identified between groups. Conclusion: Compared to other major classes of hypertensive agents, starting beta-blockers was associated with more common and earlier initiation of a loop diuretics in a population without heart failure at baseline. This finding may suggest beta-blocker induced heart failure in a population with a predominantly normal ejection fraction.

Abstract 17470: Racial Disparities in Goal Directed Medical Therapy in Patients With Systolic Heart Failure- A Single Center Study

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Ayesha Azmeen ◽  
Naga Vaishnavi Gadela ◽  
Vergara Cunegundo
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Racial Disparities ◽  
Beta Blockers ◽  
Systolic Heart Failure ◽  
The United States ◽  
Clinical Syndrome ◽  
Single Center ◽  
Geographic Variations ◽  
Reduced Ejection Fraction

Introduction: Heart failure(HF) is a clinical syndrome that is widely prevalent affecting approximately 6.5 million people in the United States. It accounts for the ever-rising health care costs in the US due to recurrent hospitalizations. Despite advancements in medical management, the mortality and the rate of hospitalizations continues to be high with geographic variations and racial disparities. Through this descriptive study, we sought to analyze the health disparities among Hispanic, African American (AA) and Caucasian population in a single-center. Methods: We identified a total of 178 patients with HF with reduced ejection fraction from our outpatient clinic by utilizing the ICD-10 codes. Patients with ejection fraction >50% have been excluded. A retrospective chart review of their ethnic background, medications, and number of heart failure exacerbations per year has been performed. Results: 178 patients (mean age 62 years, 35.56% of females) including Hispanics (n=102), AA(n=44), and Caucasians (n=32) were included in the study. Although all patients were started on Beta-blockers, only 76.4% and 37.2% of Hispanics were started on ACEi/ARBs and spironolactone respectively. Similarly, 72.7% and 45.4% of AA were started on ACEi/ARBs and spironolactone respectively. This is in contrast to Caucasians population, where a majority of patients were on started on GDMT; 90% and 75% were started on ACEi/ARBs and spironolactone respectively. This was also reflected by the number of admissions due to HF exacerbations which ranged from 2-4/year for Hispanics and AA populations and 0-1/year for Caucasians. Conclusions: GDMT for HF is known to reduce heart failure exacerbations, mortality and the ever rising cost of the healthcare system. We have observed that despite recommendations to initiate GDMT in all patients with HF with reduced ejection fraction, racial disparities exist. Physicians should be mindful of initiating GDMT in all patients.

Abstract P024: Pharmacological Treatment of Hypertension and Lv Dysfunction Predictors in ESRD Patients With AV Fistula

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sayed Tariq ◽  
James Anderson ◽  
Rohit Dhingra ◽  
Mikhail Torosoff
Keyword(s):  
Systolic Function ◽  
Beta Blockers ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Channel Blockers ◽  
Ca Channel ◽  
Av Fistula ◽  
Fistula Surgery ◽  
Lv Dysfunction ◽  
Ca Channel Blockers

Background: Effects of anti-hypertensive medications on left ventricular dimensions and systolic function in patients with arterio-venous (AV) fistulas have not been well investigated. Material and Methods: Medical charts and echocardiograms of 346 patients with AV fistula were reviewed. Of 346, 149 patients had TTE prior to the AV fistula surgery, 197 had TTE after the AV fistula surgery, and 76 patients had TTE before and after the AV fistula surgery. Data on medication use was available in 314 patients. ANOVA, chi-square, and logistic regression tests were employed. Results: In patients scheduled for AV fistula placement, 20% (31/149) patients had systolic dysfunction and 15% (22/142) had increased LV end-diastolic dimensions (LVEDD). Moderate systolic LV dysfunction was observed in 6% (9/149) and additional 8% (12/149) had severe LV dysfunction. Increased LVEDD with some LV dysfunction was noted in 27% (38/142).Following the AV fistula placement, 18% (36/197) of patients had systolic dysfunction and 12% (22/187) had increased LV end-diastolic dimensions (LVEDD). Moderate or severe systolic LV dysfunction was observed in 6% (5/197). LV systolic dysfunction or dilatation was noted in 23% (43/187). Of 314 patients, 63% were on beta-blockers (BB), 25% were on ACE inhibitor or an ARB , 43% on calcium-channel blocker , and 15% on alpha-antagonist . BB, ACEi-ARB, or AA were not associated with increased LVEDD or systolic dysfunction before or after the AV fistula placement. Prior to AV fistula, CCB treatment was not related to LV dilatation (36% in each group, p=0.981) Post AV fistula, CCB treatment was associated with increased LV dimensions (71% vs. 46%, p=0.029) but not LV systolic dysfunction (49% in LV dysfunction vs. 38% in the rest, p=0.446) . This association persisted after adjustment for co-morbidities and demographic parameters. Conclusions: LV systolic dysfunction and/or dilatation are common in patients undergoing AV fistula surgery. Despite decreased use of Ca-channel blockers in patients with LV dysfunction prior to AV fistula, Ca-channel blockers are associated with increased LV dimensions post AV fistula, and probably should be avoided in this vulnerable patient population.

scholarly journals Capabilities of Cardioprotective Therapy in the Treatment and Prevention of Heart Failure in the Postinfarction Period

2020 ◽  
pp. 7-26
Author(s):  
Valerii Batushkin
Keyword(s):  
Heart Failure ◽  
Antihypertensive Drugs ◽  
Diastolic Pressure ◽  
Beta Blockers ◽  
Stress Test ◽  
Group Versus ◽  
Stage I ◽  
Lipid Lowering ◽  
Treatment And Prevention ◽  
Hawthorn Extract

Recently, numerous and quite convincing data has been accumulated on the effectiveness and safety of lipid-lowering drugs, beta-blockers, antiplatelet and antihypertensive drugs in patients with chronic heart failure (CHF), depending on the origin of the latter. The practitioner is suggested to use several drugs of different classes at the same time in order to reduce cardiovascular mortality, as well as the risk of recurrent myocardial infarction and ischemic stroke. In CHF, metabolism in cardiomyocytes varies depending on the stage of the disease. The changes that occur in the postinfarction period are compensatory in nature, which contributes to the partial improvement of impaired metabolism, while others, on the contrary, further inhibit the processes of energy production in the myocardium. In our research paper we will discuss some capabilities of metabolic therapy of CHF and prospects in the treatment and prevention using hawthorn extract; analyze the features of interaction of some well-known cardioprotective drugs with long-term antiplatelet therapy in the postinfarction period. Initiation of therapy with a new drug in addition to clopidogrel, such as trimetazidine, may adversely affect antiplatelet activity of clopidogrel (TRACER study, 2019). As a compromise, some herbal cardioprotective drugs may be used. Hawthorn preparations containing vaso- and cardioactive substances have significant potential in the treatment of cardiovascular diseases. Diversified mechanism of action of hawthorn has a significant impact on various parts of the cardiovascular system. Clinical trials of more than 4,000 patients confirm that standardized hawthorn extracts are effective as adjunctive therapy in the treatment of NYHA stage I–III CHF. The main two-year results of the WISO cohort study showed that the three pivotal symptoms of heart failure — fatigue (p = 0.036), stress dyspnea (p = 0.020) and palpitations (p = 0.048) — were significantly less marked after treatment in the hawthorn group versus comparative group. Cochrane analysis (2009) of studies investigating hawthorn extract included 14 studies where hawthorn was used primarily as an adjunct to conventional treatment. Exercise tolerance increased significantly during the treatment with hawthorn extract. Thus, the weighted difference between the average double multiplication rates during cardiac stress test (CST) was 122.76 W/min, whereas end-diastolic pressure in the right ventricle and myocardial oxygen consumption decreased with hawthorn treatment (a weighted mean difference was 19.22 mmHg per 1 min). The reported side effects were infrequent, mild and transient. A special hawthorn extract is indicated for the treatment of patients with NYHA stage II heart failure as an alternative and supplement to the standard evidence-based drug therapy. The beneficial effect on clinical symptoms allowed patients in the Crataegus group to reduce the use of angiotensin-converting enzyme (ACE) inhibitors from 54 to 36% (p = 0.004), cardiac glycosides from 37 to 18% (p = 0.001), diuretics from 61 to 49% (p = 0.061), beta-blockers from 33 to 22% (p = 0.052). At the same time, SPICE and HERB CHF studies show greater efficacy of Crataegus preparations in the treatment of mild to moderate heart failure (NYHA stage I–II). Higher doses (1800 mg) may be required for critically ill patients in order to achieve sustained improvement. Analysis of the data available to date is promising but suggests the need for a more focused approach to dosing based on the disease severity.

scholarly journals The risk of developing chronic heart failure in patients with hypertension depending on the actual arterial stiffness

2020 ◽  
Vol 35 (2) ◽  
pp. 98-105
Author(s):  
A. I. Chernyavina ◽  
N. A. Koziolova
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Arterial Stiffness ◽  
Left Ventricular ◽  
Myocardial Mass ◽  
Developing Heart ◽  
Group 2 ◽  
Lv Volume ◽  
Lv Diastolic Function ◽  
Group 1

Objective. To determine the risk of developing chronic heart failure (CHF) in patients with hypertension (HTN) depending on the actual arterial stiffness.Material and Methods. The study included 175 patients with HTN without a verified diagnosis of heart failure. The average age was 48.5 ± 6.8 years. Patients underwent general clinical examination, volume sphygmoplethysmography assessments of cardio-ankle vascular index (CAVI), echocardiography study (left ventricular (LV) ejection fraction, LV diastolic function, LV myocardial mass index, indexed LV volume by echocardiography), and tests for serum N-terminal pro-B-type natriuretic peptide (NT-proBNP). Patients were divided into two groups depending on CAVI. Group 1 included 141 (80.6%) patients with CAVI < 9; group 2 included 34 (19.4%) patients with CAVI > 9.Results. In patients of group 1, the level of NT-proBNP was 0.008 [0.006; 5.770], which was significantly lower than the corresponding value in group 2, where the level of NT-proBNP was 13.08 [0.01; 350.65] ng/mL (p = 0.041). Indicators of odds ratio (OR) and relative risk (RR) were also significant. The chance of developing CHF with CAVI > 9 increased by almost 7 times (OR = 6.9; 95% CI = 2.8–16.8), and OR of CHF onset was 4.1 (95% CI = 2.2–7.6). Sensitivity and specificity rates were 55.9% and 84.4%, respectively. Correlation analysis revealed a medium degree of dependence and direct relationships between NT-proBNP level and CAVI values (r = 0.35; p <0.05).Conclusion. Serum level of NT-proBNP depended on the actual arterial stiffness. Patients with CAVI > 9 indicative of an increase in true arterial stiffness had a greater risk of developing heart failure assessed based on the level of NT-proBNP in the blood. Further studies are required to assess the effects of arterial stiffness, registered within the intermediate values of CAVI index, on the risk of heart failure onset. 

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