Recurrent Heart Failure Research Articles

Effects of canagliflozin on total heart failure events across the kidney function spectrum: Participant-level pooled analysis from the CANVAS Program and CREDENCE trial.

People with type 2 diabetes (T2D) face high risks of heart failure (HF) hospitalizations that are often recurrent, especially as kidney function declines. We examined the effects of canagliflozin on total HF events by baseline kidney function in patients with T2D at high cardiovascular risk and/or with chronic kidney disease. Leveraging pooled participant-level data from the CANVAS programme (n = 10 142) and CREDENCE trial (n = 4401), first and total HF hospitalizations were examined. Cox proportional hazards models were built for the time to first HF hospitalization, and proportional means models based on cumulative mean functions were used for recurrent HF hospitalizations. Treatment effects were evaluated overall as well as within baseline estimated glomerular filtration rate (eGFR) strata (<45, 45-60, and >60 ml/min/1.73 m2). HF hospitalizations were independently and blindly adjudicated. Among 14 540 participants with available baseline eGFR values, 672 HF hospitalizations occurred over a median follow-up of 2.5 years. Among participants who experienced a HF hospitalization, 357 had a single event (201 in placebo-treated patients and 156 in canagliflozin-treated patients), 77 had 2 events, and 39 had >2 events. Canagliflozin reduced risk of first HF hospitalization (hazard ratio 0.58, 95% confidence interval [CI] 0.48-0.70) consistently across baseline eGFR strata (pinteraction = 0.84). Canagliflozin reduced total HF hospitalizations overall (mean event ratio 0.63, 95% CI 0.54-0.73) and across eGFR subgroups (pinteraction = 0.51). Canagliflozin also reduced cardiovascular death and total HF hospitalizations (mean event ratio 0.72, 95% CI 0.65-0.80) and across eGFR subgroups (pinteraction = 0.82). The absolute risk reductions were numerically larger, and numbers needed to treat were smaller when evaluating total events versus first events alone. These observed HF benefits were highly consistent across the range of eGFR, with larger absolute benefits in participants who had worse kidney function at baseline. In individuals with T2D at high cardiovascular risk and/or with chronic kidney disease, canagliflozin reduced the total burden of HF hospitalizations, with consistent benefits observed across the kidney function spectrum. ClinicalTrials.gov Identifier: CANVAS (NCT01032629), CANVAS-R (NCT01989754), CREDENCE (NCT02065791).

Reassessing heart failure therapy in Thailand: Patient insights and treatment outcomes from the Thai heart failure registry

BackgroundThis research analyzed the demographics, management, and outcomes of patients with heart failure (HF) in Thailand. MethodsThe Thai Heart Failure Registry prospectively enrolled patients diagnosed with HF from 36 hospitals in Thailand. Follow-up data were recorded at 6, 12, 18, and 24 months. This study primarily focused on two outcomes: mortality and HF-related hospitalizations. ResultsThe study included 2639 patients aged at least 18. Their mean age was 59.2 ± 14.5 years, and most were male (68.4%). Patients were classified as having HF with reduced ejection fraction (HFrEF, 80.7%), HF with preserved ejection fraction (HFpEF, 9.0%), or HF with mildly reduced ejection fraction (HFmrEF, 10.3%). Guideline-directed medical therapy utilization varied. Beta-blockers had the highest usage (93.2%), followed by mineralocorticoid receptor antagonists (65.7%), angiotensin-converting enzyme inhibitors (39.3%), angiotensin receptor blockers (28.2%), angiotensin receptor-neprilysin inhibitors (16.1%), and sodium-glucose cotransporter-2 inhibitors (8.0%). The study monitored a composite of mortality and HF incidents, revealing incidence rates of 11.74, 12.50, and 8.93 per 100 person-years for the overall, HFrEF, and HFmrEF/HFpEF populations, respectively. ConclusionsDespite high guideline-directed medical therapy adherence, the Thai Heart Failure Registry data revealed high mortality and recurrent HF rates. These findings underscore limitations in current HF treatment efficacy. The results indicate the need for further investigation and improvements of HF management to enhance patient outcomes.

Prediction of recurrent heart failure hospitalizations and mortality using the echocardiographic Killip score.

Examine the performance of a simple echocardiographic "Killip score" (eKillip) in predicting heart failure (HF) hospitalizations and mortality after index event of decompensated HF hospitalization. HF patients hospitalized at our facility between 03/2019-03/2021 who underwent an echocardiography during their index admission were included in this retrospective analysis. The cohort was divided into 4 classes of eKillip according to: stroke volume index (SVI) < 35ml/m2 > and E/E' ratio < 15 > . An eKillip Class I was defined as SVI ≥ 35ml/m2 and E/E' ≤ 15 and was used as reference. Included 751 patients, median age 78.1 (IQR 69.3-86) years, 59% men, left ventricular ejection fraction 45 (IQR 30-60)%, brain natriuretic peptide levels 634 (IQR 331-1222)pg/ml. Compared with eKillip Class I, a graded increase in the combined endpoint of 30-day mortality and rehospitalizations rates was noted: (Class II: HR 1.77, CI 0.95-3.33, p = 0.07; Class III: HR 1.94, CI 1.05-3.6, p = 0.034; Class IV: HR 2.9, CI 1.64-5.13, p < 0.001 respectively), which overall persisted after correction for clinical (Class II: HR 1.682, CI 0.9-3.15, p = 0.105; Class III: HR 2.104, CI 1.13-3.9, p = 0.019; Class IV: HR 2.74, CI 1.54-4.85, p = 0.001 respectively) or echocardiographic parameters (Class II: HR 1.92, CI 1.02-3.63, p = 0.045; Class III: HR 1.54, CI 0.81-2.95, p = 0.189; Class IV: HR 2.04, CI 1.1-3.76, p = 0.023 respectively). Specifically, the eKillip Class IV group comprised one-third of the patient population and persistently showed increased risk of 30-day HF hospitalizations or mortality following multivariate analysis. A simple echocardiographic score can assist identifying high-risk decompensated HF patients for recurrent hospitalizations and mortality.

Evaluating hemoglobin thresholds for blood transfusions in oncology patients admitted in the intensive care unit.

e23319 Background: Current guidelines recommend transfusing at a hemoglobin (Hb) threshold of 7g/dl. There is a lack of evidence to support a specific threshold for transfusion in patients with active malignancy admitted to the Intensive Care Unit (ICU). This study attempts to determine an evidence-based threshold for blood transfusions in cancer. Methods: A retrospective study was done to study 561 patients with an active cancer diagnosis admitted to Northeast Georgia Medical Center ICU between 2017 and 2023 that received at least one unit of blood transfusion. Chi-Square test of association with Bonferoni correction was applied to the top five common cancers seen in ICU: Leukemia, Lymphoma, Brain tumors, Lung cancers, and GI cancers. It compared three thresholds of transfusion and looked for any change in mortality risk, readmissions, need for multiple transfusions, prevalence of new onset or recurrent heart failure, development of altered mental status, or cardiac arrest. The three thresholds for transfusions that were studied were &lt; 7g/dL, &lt; 8 g/dL, and &gt; 8 g/dL. The studied cancer types were further divided into either hematologic or solid tumors. Results: There was a decrease in overall cancer readmissions compared to expected over 30 days by 64%, 60 days by 44%, and 90 days by 47.5% when transfused for a Hb threshold of &lt;8 g/dL compared to an increase of 22.8%, 18.2%, and 18.8% in 30-, 60-, and 90-day readmissions when transfused for a Hb threshold of &lt;7 g/dL. When divided by cancer types, there was a significant decrease from expected by 30%, 47.5%, and 56% in 30-, 60-, and 90-day readmissions for patients with solid tumors for a Hb threshold of &lt; 8 g/dL. Mortality risk decreased by 50% and the need for multiple transfusions decreased by 21% when transfused for a Hb threshold of &lt; 8 g/dl. Of note, there was no significant association between transfusion levels and associated reactions. There was a decrease of 82% in altered mental status when transfused for threshold of Hb &lt;8 g/dL. Finally, significant association was not found with AKI, cardiac arrest, or heart failure and any Hb transfusion thresholds. Conclusions: Based on these results, there is a significant mortality benefit and decreased length of stay for cancer patients admitted to ICU when blood transfusion is undertaken at a hemoglobin threshold of &lt;8g/dL. These results should be further investigated in a randomized controlled trial.

Association of Paroxysmal Versus Persistent Atrial Fibrillation with In-hospital Outcomes and 30-day Readmission After Inpatient Atrial Fibrillation Ablation.

Knowledge of the impact of paroxysmal and persistent atrial fibrillation (AF) after catheter ablation on in-hospital outcomes and 30-day readmission remains limited. This study aimed to evaluate the procedural outcomes and 30-day readmission rates among patients with paroxysmal or persistent AF who were hospitalized for AF ablation. Using the Nationwide Readmissions Database, our study included patients aged ≥18 years with AF who were hospitalized and underwent catheter ablation during 2017-2020. Then, we compared the in-hospital procedural outcomes and 30-day readmission rates between patients with paroxysmal and persistent AF, respectively. Our study included 7310 index admissions for paroxysmal AF ablation and 9179 index admissions for persistent AF ablation. According to our analysis, there was no significant difference in procedural complications-namely, cerebrovascular accident, vascular complications, major bleeding requiring blood transfusion, phrenic nerve palsy, pericardial complications, and systemic embolization-between the persistent and paroxysmal AF groups. There was also no significant difference in early mortality between these groups (0.5% vs. 0.7%; P = .22). Persistent AF patients had significantly higher rates of prolonged index hospitalization (9.9% vs. 7.2%; P < .01) and non-home discharge (4.8% vs. 3.1%; P < .01). The 30-day readmission rates were comparable in both groups (10.0% vs. 9.5%; P = .34), with recurrent AF and heart failure being two of the most common causes of cardiac-related readmissions. Catheter ablation among hospitalized patients with paroxysmal or persistent AF resulted in no significant difference in procedural complications, early mortality, or 30-day readmission. This suggests that catheter ablation of AF can be performed with a relatively similar safety profile for both paroxysmal and persistent AF.

Heart failure promotes multimorbidity through innate immune memory.

Patients with heart failure (HF) often experience repeated acute decompensation and develop comorbidities such as chronic kidney disease and frailty syndrome. Although this suggests pathological interaction among comorbidities, the mechanisms linking them are poorly understood. Here, we identified alterations in hematopoietic stem cells (HSCs) as a critical driver of recurrent HF and associated comorbidities. Bone marrow transplantation from HF-experienced mice resulted in spontaneous cardiac dysfunction and fibrosis in recipient mice, as well as increased vulnerability to kidney and skeletal muscle insults. HF enhanced the capacity of HSCs to generate proinflammatory macrophages. In HF mice, global chromatin accessibility analysis and single-cell RNA-seq showed that transforming growth factor-β (TGF-β) signaling was suppressed in HSCs, which corresponded with repressed sympathetic nervous activity in bone marrow. Transplantation of bone marrow from mice in which TGF-β signaling was inhibited similarly exacerbated cardiac dysfunction. Collectively, these results suggest that cardiac stress modulates the epigenome of HSCs, which in turn alters their capacity to generate cardiac macrophage subpopulations. This change in HSCs may be a common driver of repeated HF events and comorbidity by serving as a key carrier of "stress memory."

The Challenges of Aortic Valve Management After Left Ventricular Assist Device Implantation

BackgroundContinuous retrograde flow across the aortic valve from left ventricular assist device (LVAD) therapy can result in cusp damage and progressive aortic regurgitation, potentially triggering recurrent heart and multiorgan failure. The management of aortic regurgitation after LVAD implantation has not been well defined. MethodsThis study retrospectively reviewed the investigators’ experience with the management of de novo aortic regurgitation requiring intervention in patients with continuous-flow LVAD. ResultsSix patients who had undergone LVAD implantation and who required intervention were identified. Two patients underwent redo sternotomy with bioprosthetic aortic valve replacement, and 4 patients underwent percutaneous management, including Amplatzer device (Abbott) placement and transcatheter aortic valve replacement. All patients had resolution of aortic regurgitation with improved hemodynamics and relief from heart failure. One early and 2 late deaths occurred. Valve function was intact, with all valves opening intermittently without greater than trivial aortic regurgitation. ConclusionsMultiple treatment modalities exist for LVAD-induced aortic valve regurgitation, including open surgical and percutaneous strategies. With a tailored risk-adjusted approach, acceptable results may be achieved.

Association of serum Sodium with mortality in patients of Congestive heart failure

Objectives: To determine the association of serum Sodium with mortality in patients of Congestive heart failure. Study Design: Prospective observational study Settings and Duration of study: Department of Medicine, Sir Ganga Ram Hospital, Lahore. ( 22-12-2021 to 22-6-2022 ). Methods: Sample size of 100 patients; 50 in each group in calculated with 90% power of study, 5% significance level and taking percentage of mortality i.e. 24.75% patients with low serum sodium level and in 4.21% patients with normal serum sodium level. Sample Selection: Inclusion Criteria: Patients aged between 30-70 years, both genders, Patients with congestive heart failure ,Group I: with serum sodium level &lt;135 mEq/L, Group II: with serum sodium level ≥135 mEq/L. Exclusion Criteria: Liver disorders (AST&gt;25IU, ALT&gt;30IU, hepatitis B or C), renal disorders (eGFR ˂ 30 mL/min/1.73 m2 or creatinine &gt;2.0mg/dl or on hemodialysis), any malignancy, anemia (Hb&lt;9 g/dl), due to inherited hemoglobinopathy such as; sickle cell disease, and thalassemia, Patients with recurrent congestive heart failure or already taking treatment for deranged sodium level , valvular heart disease. Results: Patients in exposed group had 52% mortality rate as compared to unexposed group in which mortality rate was only 18% respective. Value of relative risk showed that patients in exposed group had 2.88 times higher chances of mortality as compared to those patients in unexposed group. Similarly, elderly patients (Relative Risk=3.23), Male patients (Relative Risk= 3.37), Overweight patients (Relative Risk=3.54), non-diabetic patients (Relative Risk=3.50), hypertensive patients (Relative Risk=2.95), ischemic heart disease patients (Relative Risk=4.12), Smoker (Relative risk=4.41) and duration of congestive HF as 0.5-3.5 (Relative Risk= 3.03) had higher risk for mortality. Conclusion: Results obtained from this study showed that low serum sodium level had significant impact on patients of congestive HF in terms of mortality. Keeping its prognostic importance, congestive HF patients should be strictly monitored for electrolyte imbalance. Key Words: Serum sodium, Prognostic, Indicator, Mortality,Congestive Heart Failure.

Early Initiation of SGLT2 Inhibitor is Important Irrespective of Ejection Fraction

Introduction Sodium Glucose Cotransporter inhibitor (SGLTi) has revolutionized the medical management of heart failure in the last decade. This molecule was initially described as a glucose-lowering agent but now it has been recommended in patients with chronic heart failure irrespective of ejection fraction and diabetic status. SGLT2 inhibitor reduces preload by natriuresis and diuresis, reduces afterload, decreases pulmonary artery pressure, improves myocardial energetics, and decreases myocardial fibrosis. It also reduces NTpro BNP levels in heart failure patients, decreases serum uric acid, and promotes weight loss. It has also been proposed that this molecule has a favorable effect on vascular remodeling. SGLT-2i improves cardiac output and attenuates maladaptive cardiac remodeling, chronic inflammation, oxidative stress, and endothelial dysfunction (ED) by restoring the activity of nitric oxide (NO) within the vascular endothelium. As was foreseeable this molecule became one of the foundation pillars in the management of heart failure with reduced as well as preserved ejection fraction. SGLT2i also has a reno-protective effect, particularly in patients with heart failure and diabetes. Evidence with SGLT2 inhibitor in Heart failure with preserved ejection fraction (HFpEF) DELIVER TRIAL has evaluated the effect of dapagliflozin on total (first and recurrent) heart failure events in patients with heart failure having preserved ejection fraction (HFpEF) or mildly reduced ejection fraction (HFmrEF). A total of 6263 patients with LVEF of more than 40 %, NHYA Class II-IV, and high NT-pro BNP (&gt;300pg/ml in sinus rhythm and &gt; 600pg/ml in patients with atrial fibrillation) were included over the total study period of two years. Dapagliflozin 10 mg was compared to placebo. In patients with HFmrEF and HFpEF, dapagliflozin reduced the risk of total heart failure events and heart failurerelated hospital admissions. (1)

Transition from asymptomatic to symptomatic systolic chronic heart failure: rationale and design of TransitionCHF.

Chronic systolic heart failure (CHF) is a major health burden. A relevant number of patients shows asymptomatic left ventricular dysfunction (ALVSD) before symptomatic CHF or becomes asymptomatic after initiating heart failure therapy. Clinical course, prognosis, and response to pharmacological and device-based treatment are largely unknown in these two distinct groups of patients. Current pharmacological and interventional therapies do neither properly address the underlying pathophysiology nor prevent malignant loss of function. New therapeutic paradigms are needed to stop the progression from asymptomatic to symptomatic heart failure. Key questions are what causes progression of clinically asymptomatic New York Heart Association (NYHA) I heart failure to overt heart failure (>NYHA I) in some but not all patients and the underlying reasons for this transition. This requires the identification of disease mechanisms and biomarkers that predict outcome in well-defined cohorts for innovative preclinical and clinical trials. TransitionCHF is a prospective, multicentre, longitudinal pathophysiological evaluation cohort study in patients with asymptomatic systolic dysfunction NYHA I and left ventricular ejection fraction ≤40%. The cohort comprises both incidental findings and patients who had become asymptomatic after a previous symptomatic event. TransitionCHF has recruited 1000 patients with ALVSD caused by various aetiologies in 20 university heart failure clinics across Germany. Both patients with and without comorbidities at study entry will be recruited. Patients will be systematically investigated and followed up annually over the course of the study. The primary composite endpoint is time to hospitalization for heart failure and cardiovascular death. The secondary endpoints assess time to all-cause mortality, to cardiovascular mortality, to heart failure mortality, to all-cause hospitalization, to heart failure hospitalization, and to recurrent heart failure hospitalizations, as well as time to assist device implantation/transplantation. Additional investigations focusing on biomarkers, comorbidities, gender aspects, nutrition, and functional parameters including quality of life will be performed. TransitionCHF will provide a more thorough pathophysiological understanding of the progression of asymptomatic systolic dysfunction into symptomatic heart failure that will help develop therapies tailored to prevent progressive heart failure.

Effect of Empagliflozin on Heart Failure Outcomes After Acute Myocardial Infarction: Insights From the EMPACT-MI Trial.

Empagliflozin reduces the risk of heart failure (HF) events in patients with type 2 diabetes at high cardiovascular risk, chronic kidney disease, or prevalent HF irrespective of ejection fraction. Whereas the EMPACT-MI trial (Effect of Empagliflozin on Hospitalization for Heart Failure and Mortality in Patients With Acute Myocardial Infarction) showed that empagliflozin does not reduce the risk of the composite of hospitalization for HF and all-cause death, the effect of empagliflozin on first and recurrent HF events after myocardial infarction is unknown. EMPACT-MI was a double-blind, randomized, placebo-controlled, event-driven trial that randomized 6522 patients hospitalized for acute myocardial infarction at risk for HF on the basis of newly developed left ventricular ejection fraction of <45% or signs or symptoms of congestion to receive empagliflozin 10 mg daily or placebo within 14 days of admission. In prespecified secondary analyses, treatment groups were analyzed for HF outcomes. Over a median follow-up of 17.9 months, the risk for first HF hospitalization and total HF hospitalizations was significantly lower in the empagliflozin compared with the placebo group (118 [3.6%] versus 153 [4.7%] patients with events; hazard ratio, 0.77 [95% CI, 0.60, 0.98]; P=0.031, for first HF hospitalization; 148 versus 207 events; rate ratio, 0.67 [95% CI, 0.51, 0.89]; P=0.006, for total HF hospitalizations). Subgroup analysis showed consistency of empagliflozin benefit across clinically relevant patient subgroups for first and total HF hospitalizations. The need for new use of diuretics, renin-angiotensin modulators, or mineralocorticoid receptor antagonists after discharge was less in patients randomized to empagliflozin versus placebo (all P<0.05). Empagliflozin reduced the risk of HF in patients with left ventricular dysfunction or congestion after acute myocardial infarction. URL: https://www.clinicaltrials.gov; Unique identifier: NCT04509674.

Randomized investigation of the MitraClip device in heart failure: Design and rationale of the RESHAPE-HF2 trial design.

The safety and effectiveness of the MitraClip device to treat functional mitral regurgitation (FMR) has been tested in previous clinical trials yielding somewhat heterogeneous results in heart failure (HF) patients. Over time, the MitraClip device system has been modified and clinical practice evolved to consider also less severely diseased HF patients with FMR for this therapeutic option. The RESHAPE-HF2 trial aims to assess the safety and effectiveness of the MitraClip device system on top of medical therapy considered optimal in the treatment of clinically significant FMR in symptomatic patients with chronic HF. The RESHAPE-HF2 is an investigator-initiated, prospective, randomized, parallel-controlled, multicentre trial designed to evaluate the use of the MitraClip device (used in the most up-to-date version as available at sites) plus optimal standard of care therapy (device group) compared to optimal standard of care therapy alone (control group). Eligible subjects have signs and symptoms of HF (New York Heart Association [NYHA] class II-IV despite optimal therapy), and have moderate-to-severe or severe FMR, as confirmed by a central echocardiography core laboratory; have an ejection fraction between ≥20% and ≤50% (initially 15-35% for NYHA class II patients, and 15-45% for NYHA class III/IV patients); have been adequately treated per applicable standards, and have received appropriate revascularization and cardiac resynchronization therapy, if eligible; had a HF hospitalization or elevated natriuretic peptides (B-type natriuretic peptide [BNP] ≥300 pg/ml or N-terminal proBNP ≥1000 pg/ml) in the last 90 days; and in whom isolated mitral valve surgery is not a recommended treatment option. The trial has three primary endpoints, which are these: (i) the composite rate of total (first and recurrent) HF hospitalizations and cardiovascular death during 24 months of follow-up, (ii) the rate of total (i.e. first and recurrent) HF hospitalizations within 24 months, and (iii) the change from baseline to 12 months in the Kansas City Cardiomyopathy Questionnaire overall score. The three primary endpoints will be analysed using the Hochberg procedure to control the familywise type I error rate across the three hypotheses. The RESHAPE-HF2 trial will provide sound evidence on the MitraClip device and its effects in HF patients with FMR. The recruitment was recently completed with 506 randomized patients.

Association between the insufficient improvement of the quantitative flow ratio and worsening outcomes in ST-segment elevated myocardial infarction: a multicentre prospective cohort study.

Improved coronary physiological function after percutaneous coronary intervention (PCI) has been shown to improve prognosis in stable ischaemic heart disease, but has not yet been explored in ST-segment elevated myocardial infarction (STEMI). The study sought to determine whether an improvement in the quantitative flow ratio (QFR) could improve the prognosis of STEMI patients undergoing primary PCI. Patients diagnosed with STEMI who were receiving primary PCI were recruited for the study. Those with thrombolysis in myocardial infarction (TIMI) flow <2 after wiring were excluded. The ΔQFR was calculated using the following formula: ΔQFR = post-PCI QFR - pre-stent QFR. The primary endpoint was the composite event, including recurrent myocardial infarction (MI) and acute heart failure (AHF). In total, 515 STEMI patients with a median follow-up of 364 days were enrolled in the study. Based on the cut-off value from the receiver operator characteristic (ROC) curve, the patients were divided into the following two groups: the lower ΔQFR group (≤0.25, N=332); and the normal ΔQFR group (>0.25, N=183). Patients with a lower ΔQFR had a relatively higher rate of MI/AHF (10.5% vs. 4.4%, P=0.019) and AHF (7.2% vs. 2.7%, P=0.044). A lower ΔQFR was significantly associated with a higher incidence of MI/AHF [hazard ratio (HR) =2.962, 95% confidence interval (CI): 1.358-6.459, P=0.006, respectively] after adjusting for potential confounders. Pre-stent angiographic microvascular resistance [odds ratio (OR) =1.027, 95% CI: 1.022-1.033, P<0.001] and the stent-to-vessel diameter ratio <1.13 (OR =1.766, 95% CI: 1.027-3.071, P=0.04) were independent predictors of a lower ΔQFR. An insufficient improvement in the QFR contributes to worsening outcomes and might be a useful tool for risk stratification in STEMI.

Anaesthetic Management of a Pregnant Lady with Epstein Anomaly

Wilhelm Ebstein first described the clinical and anatomical features of an anomaly of the tricuspid valve in 1866, which occurs in 1 percent of congenital heart defects (1 in 110,000 of the general population). It is characterized by dysplastic abnormalities of both basal and free attachments of the tricuspid valve leaflets, with downward displacement and elongation of the septal and anterior cusp, with resulting tricuspid regurgitation. Congestive heart failure and sudden collapse are the most common causes of death Case Report: A 21 year old primi with 37 wks gestation was referred to our hospital for complicated pregnancy management. She complained of occasional palpitations, and dyspnoea on severe exertion. She had no history of recurrent chest infections, cyanosis or heart failure in the past. On examination she had pansystolic and mid-diastolic murmurs with right parasternal thrill, along with widely split second heart sound. The ECG showed sinus rhythm with right bundle branch block. Chest X-ray showed enlarged right atrium with cardiomegaly, while echocardiogram showed the presence of moderately enlarged right atrium, tricuspid regurgitation with downwardly displaced tricuspid valves, confirming diagnosis of Ebstein’s anomaly. Her blood reports were within normal limits. We kept ready all routine and emergency drugs and equipments. Subsequently she was shifted into the OT, monitors were attached, and given antibiotics for bacterial endocarditis prophylaxis. A sitting epidural was tried at L3-4 interspace. INJ bupivacaine 0.5% 15cc given in graded doses of 5 cc every 5 minutes by monitoring hemodynamic response. Level achieved till T6. Thereafter left lateral tilt and oxygen were continuously administered to the patient. Intraoperatively her vitals were stable and duration of operation was 60 minutes and a female baby of birth weight 2.4kg was extracted. Postoperatively the patient vitals were stable. Conclusion: In conclusion, women with Ebstein’s anomaly may present with a multitude of problems and, should be considered as high risk and cared for in tertiary centres by a multidisciplinary team including obstetricians, cardiologists and obstetric anaesthetists in pregnancy and during delivery. Epidural anaesthesia in a fractionated or ‘graded’ manner provides a haemodynamically stable patient with adequate analgesia, and may be preferred to general anaesthesia in these patients.

Double Intervention in a Patient with Large Patent Ductus Arteriosus (PDA) and Moderate Upper Muscular Ventricular Septal Defect (VSD) with Bidirectional Shunt with Severe Pulmonary Hypertension

Patent ductus arteriosus (PDA) and Ventricular septal defect (VSD) are commonly encountered problems and constitute about 40% of all congenital heart lesions. The association of these two conditions in a single patient is not very uncommon. Both these conditions can be treated by placing intracardiac devices. Double interventional closure of Patent Ductus Arteriosus (PDA) and Ventricular Septal Defect (VSD) was performed in a gravely ill infant at her 3 months and 5 months of age respectively, who was suffering from recurrent pneumonia and heart failure since birth. These were lifesaving procedure for that patient which led to writing this report.

Study of clinical profile of patients with acute coronary syndrome and the correlation of serum fibrinogen and grace score as a prognostic marker for predicting 3-month mortality

Introduction. Acute coronary syndrome (ACS), encompassing unstable angina, non-ST-segment eleva­tion myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI), is a major global health concern due to its high morbidity and mortality. Research highlights a link between ACS and elevated acute phase reactants like C-reactive protein, emphasizing the role of inflammation and atherosclerosis. Serum fibrinogen, crucial in thrombus formation and an inflammatory marker, is significant in the coagu­lation process. This study investigates the predictive value of serum fibrinogen levels and the GRACE score for 3-month mortality in ACS patients. Aim. To examine the clinical profile of ACS patients and evaluate serum fibrinogen and GRACE score as prognostic markers for 3-month mortality. Methodology. A prospective observational study was conducted on 50 patients diagnosed with ACS at Saveetha Medical College Hospital. The study included adults over 18 with ACS, excluding those with severe comorbid conditions like end-stage liver disease or malignancy. Serum fibrinogen levels were measured at presentation and at 3 months using an automated coagulation analyzer. GRACE scores were calculated, and clinical assessments including ECG, cardiac markers, and ECHO were conducted. Data analysis involved IBM SPSS Statistics, utilizing descriptive statistics, t-tests, ANOVA, and Pearson's Correlation. Results. The study group had diverse demographics and a high prevalence of cardiovascular symptoms and comorbidities. The clinical profile of ACS showed a higher incidence of STEMI. Serum fibrinogen levels varied significantly across different Killip classes at presentation and at 3 months, with the highest levels in the more severe classes. Higher serum fibrinogen was linked to recurrent heart failure admissions and higher KILIPS class. However, there was no significant difference in fibrinogen levels between patients with and without interventions. The GRACE score was higher in STEMI patients, those with LV dysfunction, and correlated with higher serum fibrinogen. Lower FACIT F scores, indicating higher fatigue, were associated with higher fibrinogen levels and readmissions for heart failure. Conclusion. Higher serum fibrinogen levels and GRACE scores at presentation and at three months are indicators of severe myocardial infarction, increased heart failure readmission rates, and greater fatigue in ACS patients. These markers are valuable for evaluating morbidity in ACS and can aid in enhancing patient management strategies.

Mean Platelet Volume and Its Association With In-Hospital Outcomes in Patients With Acute ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

Background Mean platelet volume (MPV), reflecting platelet size and activation, has been associated with cardiovascular disease (CVD) risk and mortality. Yet, its prognostic significance in acute coronary syndrome (ACS) patients undergoing primary percutaneous coronary intervention (PCI) remains uncertain. This study investigates whether elevated MPV levels upon admission in ST-segment elevation myocardial infarction (STEMI) patients predict adverse in-hospital outcomes after primary PCI. Objectives The aim of this study was to measure MPV in patients with STEMI who underwent primary PCI and to evaluate its association with in-hospital outcomes such as death, recurrent myocardial infarction, heart failure, and bleeding. Methods We enrolled 400 consecutive patients with STEMI (mean age 56.20 years, 356 males, 44 females) who underwent primary PCI at our center. We obtained MPV values from complete blood count tests performed at admission. We divided the patients into two groups based on the normal MPV range of 7.40 to 12 fL. We compared the baseline characteristics and in-hospital outcomes of the two groups. We used Cox proportional hazards regression analysis to adjust for potential confounders and evaluate the impact of MPV on in-hospital outcomes. Results There was no significant difference in MPV values between the two groups (9.10 ± 1.20 fL vs. 9.00 ± 1.10 fL, p = 0.54). Patients who died exhibited higher age, male predominance, hypertension, diabetes, a lower left ventricular ejection fraction, lower levels of low-density lipoprotein cholesterol, and lower levels of hemoglobin and hematocrit compared to survivors. MPV was not associated with any of the in-hospital outcomes in the unadjusted or adjusted analyses. Conclusion In this cohort of patients with STEMI who underwent primary PCI, admission MPV was not a predictor of in-hospital outcomes. Further studies are needed to clarify the role of MPV in the pathophysiology and prognosis of ACS.

Daprodustat and Heart Failure in CKD.

Patients with chronic kidney disease (CKD) are at higher risk for heart failure. The hypoxia inducible factor prolyl hydroxylase inhibitor daprodustat is an orally acting alternative to conventional injectable erythropoietin-stimulating agents (ESA) for the treatment of anemia in patients with CKD. Whether daprodustat affects the risk of heart failure hospitalization is unknown. The ASCEND-D (n=2,964) and ASCEND-ND (n=3,872) trials compared daprodustat to conventional ESA in patients with anemia of CKD who did or did not require dialysis, respectively. We identified risk factors for heart failure hospitalization and assessed the effect of daprodustat compared to conventional ESA on heart failure hospitalizations. History of heart failure, diabetes, and higher systolic blood pressure were independently associated with heart failure hospitalization in both trials, irrespective of treatment assignment. The number of first heart failure hospitalizations was greater in the daprodustat arm in patients not receiving dialysis (hazard ratio [HR] 1.22 [0.95-1.56], p=0.12] and in patients receiving dialysis (HR 1.10 [0.84-1.45], p=0.47), though these differences were not statistically significant. HRs in patients with and without history of heart failure were 1.37 (0.89-2.11) vs 1.08 (0.79-1.46) (p-interaction=0.36) in ASCEND-ND, and 1.52 (0.97-2.38) vs 0.93 (0.66-1.30) (p-interaction=0.09) in ASCEND-D, respectively. In post hoc analyses, daprodustat increased total (first and recurrent) heart failure hospitalizations in participants not receiving dialysis (rate ratio 1.46 [1.11-1.92], p=0.007) ) but not in participants receiving dialysis (rate ratio 1.01 [0.74-1.39], p=0.93). Daprodustat did not significantly affect the risk of a composite outcome of first heart failure hospitalization or death. A greater number of first heart failure hospitalization events occurred in patients treated with daprodustat compared with conventional ESA, but this difference did not reach statistical significance. Differences in the number of heart failure hospitalization events were most apparent in patients not receiving dialysis and in patients with history of heart failure.

Effect of sacubitril valsartan on heart failure with mid-range or preserved ejection fraction in patients on maintenance hemodialysis: real-world experience in a single-center, prospective study

BackgroundThis study aimed to evaluate the effect of sacubitril valsartan (SV) on heart failure (HF) hospitalization and cardiovascular mortality in patients on hemodialysis with HF with preserved ejection fraction (EF; HFpEF).MethodsThis single-center, prospective study enrolled 155 stable hemodialysis patients with EF > 40% who were followed up for 12 months. Fifty-nine patients were treated with SV; the others were matched for EF (57.89 ± 9.35 vs. 58.00 ± 11.82, P = 0.9) at a ratio of 1:1 and included as controls. The target dosage of SV was 200 mg/day.ResultsTwenty-three (23/155; 14.84%) had HF with mid-range EF (HFmrEF), while 132 (85.16%) had HFpEF. After SV treatment, the peak early diastolic transmitral flow velocity/peak early diastolic mitral annular tissue velocity(E/e’) improved from 17.19 ± 8.74 to 12.80 ± 5.52 (P = 0.006), the left ventricular (LV) end-diastolic diameter decreased from 53.14 ± 7.67 mm to 51.56 ± 7.44 mm (P = 0.03), and the LV mass index decreased from 165.7 ± 44.6 g/m2 to 154.8 ± 24.0 g/m2 (P = 0.02). LVEF (P = 0.08) and LV global longitudinal strain (P = 0.7) did not change significantly. The composite outcome of first and recurrent HF hospitalization or cardiovascular death showed no difference between group. However, the Acute Dialysis Quality Initiative Workgroup (ADQI) HF class improved in 39 and 15 patients and worsened in 1 and 11 patients in the SV and control groups, respectively (P < 0.001). Age, diabetes mellitus, and pulmonary arterial pressure were independent risk factors for HF hospitalization and cardiovascular mortality in patients with HFpEF.ConclusionsSV improved LV hypertrophy, diastolic function, and the ADQI class for HF; however, it failed to reduce the composite endpoints of HF hospitalization and cardiovascular disease-related mortality over 12 months of follow-up in patients on maintenance hemodialysis with EF of > 40%.

Delayed Diagnosis of Constrictive Pericarditis Resulting in Recurrent Heart Failure: A Case Report

Constrictive pericarditis can lead to compromised diastolic ventricular filling due to pericardial inflammation and fibrosis. A diagnosis of constrictive pericarditis was established by identifying structural and hemodynamic features through echocardiography. We present a case of constrictive pericarditis, which manifested in the form of gradually worsening dyspnea and lower-extremity edema over a 7 years period. The patient was diagnosed with constrictive pericarditis using echocardiography, and underwent a pericardiectomy.