Development Of New-onset Heart Failure Research Articles

Cardiac Manifestations of Post-Acute COVID-19 Infection.

There is emerging evidence that the post-acute and chronic phases of COVID-19 infection are associated with various significant cardiovascular sequelae. Long COVID has been shown to be associated with multiple cardiovascular sequelae including direct myocardial injury, arrhythmias, and cardiomyopathies. Hypotheses on the mechanism of myocardial injury include direct viral infiltration and autoimmune dysregulation. Long COVID is associated with persistent cardiac ischemia in patients with no previous history of coronary disease, atrial and ventricular arrhythmias, and the development of new-onset heart failure in previously healthy patients. Onset of long COVID may be related to severity of the initial SARS-CoV2 infection. Cardiac MRI is a valuable tool in assessing myocarditis and the development of cardiomyopathies in the setting of long COVID. Both patients with and without pre-existing cardiovascular disease are at risk of developing myocardial injury in the setting of long COVID. Future studies will elucidate both cardiovascular mortality and cardiac rehabilitation in the post-acute and chronic phases of COVID-19.

Clinical impact of pulmonary hypertension on the outcomes of acute myocardial infarction patients with or without chronic obstructive pulmonary disease.

Acute myocardial infarction (AMI) and chronic obstructive pulmonary disease (COPD) are leading global causes of morbidity and mortality. In patients with both of these conditions, the presence of pulmonary hypertension (PH) can further worsen their prognosis. We examined the outcomes of AMI patients with COPD (AMI+COPD) and without COPD (AMI−COPD), depending on the presence or absence of PH.A total of 318 AMI patients with COPD (AMI+COPD cohort) (n = 109) or without COPD (AMI-COPD cohort) (n = 209) were included in this study and were subdivided into 2 groups according to right ventricular systolic pressure (RVSP) level (PH group [RVSP ≥35 mm Hg] and no PH group [RVSP <35 mm Hg]).We investigated characteristics and clinical outcomes in both the AMI-COPD and AMI+COPD cohorts. When investigating in-hospital clinical outcomes, the PH group had a higher proportion of new-onset heart failure (HF) in both cohorts. In the AMI+COPD cohort, however, the PH group had a higher incidence of cardiogenic shock than the no PH group, which was consistent with the result of the post-inverse probability of treatment weighting (IPTW) analysis. When investigating 1-year clinical outcomes, the PH group had higher incidences of a major adverse cardiac event and all-cause mortality in both cohorts. This finding was mainly driven by cardiac death in the AMI-COPD cohort, whereas it was mainly driven by non-cardiac death in the AMI+COPD cohort. After IPTW adjustment, these differences were statistically attenuated such that all variables were similar between both groups.PH may be associated with the development of new-onset HF (in all patients) and cardiogenic shock (in the AMI+COPD cohort). In addition, PH may be also associated with all-cause mortality, although it was statistically attenuated after IPTW adjustment.

Abstract 15488: Epidemiological Profile of Cardiovascular Risk Factors and Outcomes in Patients With Solid Organ and Haematological Malignancies

Introduction: Chemotherapy remains the cornerstone in the management of solid organ malignancies (SOM) and hematological malignancies (HM). Although life-prolonging, it is not without cost, with heart failure and arrhythmia becoming increasingly recognised complications of treatment. Although there is significant overlap in the chemotherapeutic management of SOM and HM, epidemiological information on the differential prevalence of baseline cardiovascular risk factors and outcomes in these populations is scarce. Hypothesis: A differential cardiovascular risk profile and clinical course will be appreciated in patients with SOM and HM undergoing chemotherapy. Methods: Retrospective observational study design. Patients admitted to our institution undergoing chemotherapy for SOM (2014-2018) or HM (2012-2015) were reviewed. Baseline demographic and clinical data was collated and patients were followed for up to five years following chemotherapy for occurrence of major adverse cardiac events (MACE) defined as the development of new-onset heart failure or arrhythmia. Results: 545 hematology and 435 oncology patients with malignancy were assessed. Compared to those with HM, those treated for SOM had a poorer cardiovascular risk profile (table 1). At mean follow-up period of 22.8±17.8 months, no significant difference in the incidence of the composite endpoint (9.4% vs 9.0%, p=0.45) or its components was observed. Higher rates of anthracycline therapy was observed in patients with HM (100% vs 17%, p &lt; 0.01), however its use did not have a differential effect on MACE (12% vs 9%, p=0.25). Conclusions: Compared to patients treated for HM, patients with SOM had a greater burden of cardiovascular risk factors and lower use of anthracycline chemotherapy. Despite this, MACE occurred at similar rates in both groups. The use of anthracyclines was not associated with the development of MACE, suggesting alternative pathways contributing to its development.

Risk of heart failure associated with thiazide diuretics compared with calcium channel blockers in patients with type 2 diabetes: a nationwide nested case-control study

Abstract Background Thiazide diuretics and calcium channel blockers (CCB's) are two important and widely used antihypertensive drugs classes among patients with type 2 diabetes (T2D). The risk of developing heart failure (HF) is increased in patients with T2D but whether use of these two drugs are associated with changes in HF risk is unknown. Purpose To examine and compare the association of two different classes of antihypertensive drugs, thiazide diuretics and CCB's, with the development of new onset HF in patients with T2D. Methods The study cohort comprised T2D patients &amp;gt;40 years on metformin and renin-angiotensin system inhibitor (RAS-i) without a history of HF or use of loop diuretics identified in Danish health care registers (period 1995 to 2015). A nested case-control study was conducted by matching all HF cases on sex, age and duration of T2D with 10 controls from the T2D population. Exposure was defined as three redeemed prescriptions of either a thiazide diuretic or a CCB up to 365 days before index, which corresponds to one year of antihypertensive therapy. Conditional logistic regression adjusted for comorbidities (atrial fibrillation, chronic obstructive pulmonary disease and anemia) was used to estimate and compare the treatment effect of thiazide diuretics and CCB's, with patients receiving neither of the two drugs as reference. Results The study population consisted of 170,514 T2D patients using metformin and RAS-i, comprising 13,814 HF cases each matched on sex, age and duration of T2D with 10 controls. The median age was 62 years and 55% were men. T2D patients, who had received antihypertensive treatment with only thiazide diuretics one year prior to index had a significantly lower risk of HF compared to the reference group who did not receive treatment with neither thiazide diuretics or CCB's: Hazard ratio (HR) 0.79 [95% confidence interval (CI) 0.74–0.85]. Patients who had received treatment with only CCB's had a comparable risk of HF: HR 0.98 [95% CI 0.94–1.02]. Patients who had received treatment with both thiazide diuretics and CCB's were not associated with a lower risk of HF: HR 1.01 [95% CI 0.96–1.08]. Conclusion Patients with T2D who received antihypertensive therapy with thiazide diuretics for at least one year had a significantly lower risk of HF compared to those who were not treated with either thiazide diuretics or CCB's. No association between use of CCB's and HF was observed. Use of thiazide diuretics may prevent development of HF in T2D and a randomized clinical trial evaluating diuretics is patients with T2D is warranted. Risk of new onset heart failure Funding Acknowledgement Type of funding source: None

BODY MASS INDEX AND LEFT VENTRICULAR FUNCTION OF ACUTE CORONARY SYNDROME SURVIVORS: DATA FROM THE TRACE-CORE COHORT

Obesity is associated with the development of new-onset heart failure (HF). Paradoxically, in patients with chronic HF, overweight and mild obesity is associated with improved survival compared to normal weight patients. Our aim was to explore the relationship between body mass index (BMI) and left

Prognostic Implications of Serum Albumin Levels in Patients With Acute Coronary Syndromes

Hypoalbuminemia is a long-term risk factor for incident of both myocardial infarction and heart failure. We assessed whether serum albumin levels at admission are associated with new-onset heart failure and in-hospital mortality in patients with acute coronary syndrome (ACS). The study included 7,192 patients with ACS with no previous history of heart failure. Patients were divided into quartiles according to serum albumin levels (Q1: ≤3.50g/dl; Q2: 3.51 to 3.80g/dl; Q3: 3.81 to 4.08g/dl; and Q4: >4.08g/dl). Logistic regressions were used to explore the relations among serum albumin quartiles, new-onset heart failure, and in-hospital mortality. Serum albumin levels were negatively correlated with both high-sensitivity C-reactive protein and white blood cell count at admission. The unadjusted rate for both new-onset heart failure (37.7%, 20.2%, 14.7%, and 11.4% for Q1, Q2, Q3, and Q4, respectively; p <0.0001) and in-hospital mortality (9.8%, 3.4%, 2.0%, and 1.7% for Q1, Q2, Q3, and Q4, respectively; p <0.0001) were higher at lower serum albumin levels. Multivariate analysis demonstrated that serum albumin level ≤3.50g/dl is an important and independent predictor of both the development of new-onset heart failure (odds ratio 2.31, 95% CI 1.87 to 2.84, p <0.0001) and in-hospital mortality (odds ratio 1.88, 95% CI 1.23 to 2.86, p= 0.003). In conclusion, albumin level ≤3.50g/dl is an independent predictor of new-onset heart failure and in-hospital mortality in patients with ACS. The inflammatory state may be a mechanism underlying hypoalbuminemia in this clinical setting.

Hemoglobin levels and new-onset heart failure in the community

In established cardiovascular disease and heart failure (HF), low hemoglobin levels are associated with unfavorable outcome. Whether hemoglobin levels are associated with the development of new-onset HF in the population is unclear. This study sought to investigate the relationship between hemoglobin levels and development of new-onset HF in the community. In 6,744 patients from PREVEND, a prospective, community-based, cohort study, we analyzed the relationship between hemoglobin levels and the risk of new-onset HF. Mean age (±SD) was 53 ± 12 years, 49.8% was male, and mean hemoglobin level was 13.7 ± 1.2 g/dL. During a median follow-up of 8.3 years (interquartile range 7.8-8.9), 217 subjects (3.2%) were newly diagnosed with HF. The association between hemoglobin levels and the risk for new-onset HF was U shaped (P< .001), remaining significant after full adjustment in a multivariable model with established cardiovascular risk factors (P= .015). Furthermore, a increased annual HF incidence was already observed in subjects with high-normal hemoglobin levels (men >16 g/dL or women >15 g/dL; P= .041), whereas on the other side of the distribution, only severe anemia (men <11 g/dL or women <10 g/dL; P= .018) was associated with a higher annual incidence. The impact of hemoglobin level on the risk of new-onset HF in the community is best described as U shaped. Interestingly, higher hemoglobin levels, already within the high-reference range, are associated with an increased incidence. This in contrast to anemia, where a higher annual HF incidence was only observed for severe anemia.

Obesity and the Obesity Paradox in Heart Failure

Obesity is a growing public health problem in the general population, and significantly increases the risk for the development of new-onset heart failure (HF). However, in the setting of chronic HF, overweight and mild to moderate obesity is associated with substantially improved survival compared to normal-weight patients. Evidence exists for an “obesity paradox” in HF, with the majority of data measuring obesity by body mass index, but also across various less-frequently used measures of body fat (BF) and body composition including waist circumference, waist–hip ratio, skinfold estimates of percent BF, and bioelectrical impedance analysis of body composition. Other emerging areas of investigation such as the relationship of the obesity paradox to cardiorespiratory fitness are also discussed. Finally, this review explores various explanations for the obesity paradox, and summarizes the current evidence for intentional weight loss treatments for HF in context.

Incidence and predictors of heart failure hospitalization and death in permanent pacemaker patients: a single-centre experience over medium-term follow-up

The aim of this study was to assess the incidence and clinical predictors of the development of new-onset heart failure (HF) over medium-term follow-up, in patients treated with permanent pacing in daily clinical practice. We retrospectively enrolled all consecutive patients who underwent single- or dual-chamber pacemaker implantation at the study centre. Patients with a left ventricular ejection fraction (LVEF) ≤35% or a prior diagnosis of HF were excluded. Ventricular leads were routinely implanted in the right apex. Pacemakers were implanted in 490 patients with a standard pacemaker indication and LVEF >35%. Left bundle-branch block (LBBB) was reported in 30 (8%) patients, and an LVEF <50% in 64 (13%) patients. During a follow-up of 27 ± 21 months, 32 (7%) patients reached the combined endpoint of HF death or hospitalization. On multivariate analysis, LBBB (HR, 3.50; 95% CI, 1.1-11.1; P = 0.033) and LVEF <50% (HR, 5.1; 95% CI, 1.9-14.2; P = 0.002) were confirmed as independent predictors of HF death or hospitalization. Patients with LVEF <50% and/or LBBB displayed significantly higher rates of HF death or hospitalization (log-rank test, all P<0.001). The majority of patients with a standard indication for permanent pacing and normal LV function remained in a clinically stable condition after pacemaker implantation. However, ∼7% of patients developed new-onset HF over a period of follow-up of 27 months, and the presence of LBBB and LVEF <50% at the baseline predicted HF death or hospitalization.

Type 2 Diabetes Mellitus and Heart Failure

Diabetes mellitus and heart failure are common comorbidities, and their prevalence has increased significantly over the past decade. We examined the relationships between diabetes and heart failure, the effect of commonly prescribed antidiabetic drugs on the development of heart failure, and the benefits and risks of recommended heart failure therapies in patients with diabetes. Compared with patients with heart failure who do not have diabetes, patients with both diabetes and heart failure have a poorer prognosis, including a 1.5-2-fold higher risk of mortality. Based on the results of randomized controlled trials, insulin and sulfonylureas do not appear to protect against or contribute to the development of new-onset heart failure, whereas metformin may modestly reduce the risk. The use of metformin in patients with established heart failure is controversial; retrospective analyses have shown that metformin may have a beneficial effect on outcomes, but there are no prospective, randomized clinical trials to support its use in this population. The thiazolidinediones, however, contribute to the development of heart failure and increase the risk of heart failure exacerbations particularly when used in combination with insulin. Recommendations for the treatment of symptomatic heart failure in patients with diabetes have been largely derived from post hoc analyses or preplanned subgroup analyses in landmark clinical trials. The data clearly support the use of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers for both the prevention and treatment of symptomatic heart failure in patients with diabetes. Despite concerns regarding the potential risks of beta-blockers in patients with diabetes, these drugs have a clear mortality benefit in patients with stages B and C heart failure. Therefore, patients with diabetes should not be denied beta-blocker therapy unless there is a clear contraindication. Likewise, aldosterone receptor antagonists should be added to standard therapies in patients with stages C and D heart failure. Future heart failure studies should include a sufficiently large diabetes cohort to conduct meaningful preplanned subgroup analyses that examine the effect of proposed treatments on both heart failure-related and diabetes-related outcomes.