Background: Tricuspid regurgitation related to permanent pacemaker (PPM) lead can occur in 25-29% of patients compared to individuals who did not undergo such procedure, with symptoms of right heart failure developing from six months to ten years after PPM implantation. Early detection is necessary as prompt intervention maybe required to prevent morbidity and even mortality. Aim: This study has been carried out to determine the incidence and severity of pacemaker lead-related tricuspid regurgitation (TR) immediately after the procedure and 1–3 months after permanent pacemaker implantation. Methods: This is a prospective cohort study on 60 patients who underwent permanent pacemaker implantation. Baseline demographic, electrocardiographic and echocardiographic parameters were collected. Patients underwent follow-up 2D- and 3Dechocardiogram within three days or prior to discharge and within one to three months after permanent pacemaker insertion to determine the development of tricuspid regurgitation (TR) or increase in its severity from baseline. Results: The mean age was 65.2 ± 13.5 years, majority were females (58%) who underwent permanent pacemaker implantation predominantly due to advanced atrioventricular block (75%). Three patients developed mild TR and one patient developed moderate TR within three days postoperatively. On follow-up within one to three months postoperatively, thirteen patients (22%) developed moderate TR and one patient developed severe TR, which required removal of the RV lead with improvement thereafter. Conclusion: In this study cohort, nearly one-fourth of patients who underwent implantation of permanent pacemaker developed at least moderate TR within one to three months of the procedure. Follow-up echocardiogram 3 months after pacemaker implantation may be warranted to detect this complication early.

Background: Pentraxin 3 (PTX3), a member of C-reactive protein-like inflammatory protein group, is abundantly expressed in atherosclerotic plaques, as well as in cardiac myocytes. Increased serum PTX3 level has been observed in patients with the acute coronary syndrome (ACS). The diagnostic role of PTX3 in all three types of ACS in the Indian population is limited. This study aimed to investigate whether serum PTX3 can be used as a potential biomarker in the early detection of ACS. Materials and Methods: This is a cross-sectional case-control study comprising of 47 cases and 33 controls. Cases were divided into three groups, out of which 12 patients were of non-ST-segment elevation myocardial infarction (NSTEMI), 23 patients were of ST-segment elevation myocardial infarction (STEMI), and 12 patients were of unstable angina. Patients were recruited within 7 h of post event who are clinically diagnosed as ACS. Lipid parameters were measured on the Roche Cobas c511 analyzer and PTX3 levels were measured by ELISA kit. Results: Serum PTX-3 levels were significantly higher in all three groups of ACS when compared to controls (P < 0.0001). At a cutoff of 4 ng/ml, serum pentraxin-3 showed 97.87% sensitivity and 84.85% specificity in diagnosing ACS cases with a positive predictive value of 90.2% and negative predictive value of 96.6%, and the area under the curve was 0.978. At a cut-off of 3.56 and 6.09 ng/ml, serum PTX-3 has 100% sensitivity and 78.79% specificity and 91.67% sensitivity and 100% specificity in diagnosing NSTEMI and STEMI, respectively. Conclusions: This study demonstrates Pentraxin-3 levels in ACS cases were significantly high and showed as a valuable biomarker for early detection of ACS, particularly within 7 h of postevent. Assessment of pentraxin-3 and Troponin-T together may further improve the early detection of ACS patients.

Background: Systemic lupus erythematosus (SLE) is a connective tissue disorder with cardiovascular involvement associated with high morbidity and mortality. Routine echocardiography often misses early myocardial involvement. We intend to use tissue Doppler imaging (TDI), strain and strain rate imaging to reveal subclinical myocardial dysfunction in asymptomatic females with SLE; and its correlation with disease activity and anticardiolipin antibodies. Materials and Methods: Forty-three female SLE patients without cardiac symptoms or signs and matched healthy control group (n = 20) underwent standard echocardiography, TDI, strain and strain rate imaging. Disease activity of SLE was assessed using the SLE disease activity index (SLEDAI); ≥6 points were considered active. Results: Mean age of SLE patients was 29.86 years with a mean SLEDAI score of 4.36 ± 4.5. Standard two dimensional-Echocardiogram parameters were similar to healthy controls. SLE was associated with significantly impaired systolic myocardial velocities of left ventricle measured by TDI; medial S': 8.5 ± 1.2 versus 9.6 ± 1.0 cm/s, P = 0.007; lateral S': 9.2 ± 1.7 versus 11.4 ± 1.6 cm/s, P = 0.012); and decrease in strain (−17.2% ± 2.2% vs. −20.95% ± 2.1%; P < 0.001) and strain rate (P < 0.05). There was no significant difference with the presence of anti-cardiolipin antibodies. Patients with higher disease activity had decreased systolic myocardial velocity on TDI and strain imaging as compared to low activity patients. Conclusion: Asymptomatic SLE patients showed impairment of left ventricular systolic and diastolic function compared to healthy controls. TDI and strain imaging detects early subclinical myocardial involvement that correlates with disease activity. Such evidence of early myocardial involvement needs further evaluation to reclassify SLE disease activity and guide management.

Introduction: Contrast-associated acute kidney injury (CA-AKI) is a prevalent but underdiagnosed complication of percutaneous coronary intervention (PCI) that is associated with increased inhospital morbidity and mortality. Aims and Objectives: The aims and objectives were to study the incidence, risk factors, and outcome of CA-KI following PCI. Materials and Methods: This was a single-center prospective observational study. Five hundred patients who were admitted in ward and medical intensive care unit with chronic stable angina and acute coronary syndrome (unstable angina, non-ST-elevation myocardial infarction [STEMI], and STEMI) for PCI (intracoronary stent implantation) were included in the present study. All baseline demographic and clinical characteristics including pre- and postprocedure kidney function test (24 h, 48 h) were noted. Hospital stay, need for dialysis, and mortality were recorded. Results: In this study, 500 patients were enrolled. The mean age of presentation was 61.83 ± 13.17 years. Three hundred and sixty-six patients (73.2%) were male. Of 500 patients, 52 (10.4%) patients developed AKI. AKI was significantly higher in those with diabetes (27.2% vs. 5.4% P < 0.001), heart failure (23.1% vs. 6.5% P < 0.001), left ventricular (LV) dysfunction (21.6% vs. 6.3% P < 0.001), peripheral vascular disease (24.5% vs. 8.9% P = 0.002), hypotension (42.6% vs. 5.2% P < 0.001), creatinine >1.2 (18.5% vs. 5.9% P < 0.001), lower creatinine clearance < 60 (25.4% vs. 5.8% P < 0.001), higher procedural time >60 min (20.2% vs. 7.3% P < 0.001), and higher contrast volume (302.7 ± 37.83 mL in AKI patients vs. and 173.2 ± 23.61 mL in no AKI patients P < 0.001). Multivariate logistic regression analysis showed Type 2 diabetes mellitus, heart failure, LV dysfunction, creatinine clearance <60, and contrast volume more than 270 mL to be significantly associated with the incidence of CA-AKI. AKI patients had significantly prolonged hospital stay as compared to those without AKI (9.2 ± 2.73 vs. 4.7 ± 1.79 days P < 0.001). Dialysis was required only in one (1.9%) patient. AKI patients had higher in hospital mortality as compared to non-AKI group (3 [5.8%] vs. 2 [0.4%] P = 0.004). Conclusion: The incidence of AKI after PCI in our study was 10%. Patients having diabetes, heart failure, LV dysfunction, estimated creatinine clearance, and higher contrast volume were found to be at highest risk. Appropriate preventive measures should be taken in these high-risk patients to avoid adverse outcomes associated with contrast-induced nephropathy.

Background: Treatment of the left ventricular thrombus (LVT) with Vitamin K antagonists (VKAs) such as warfarin may lead to longer hospitalization. Thus, the potential of non-VKA oral anticoagulants as alternative to warfarin need to be explored. This study aims to investigate the size reduction or resolution of LVT with apixaban compared to conventional warfarin. Materials and Methods: This is a pilot, prospective, single-center, randomized, single-blinded outcome study with patients diagnosed with LVT. Patients diagnosed with LVT by echocardiography were randomized into two treatment groups: apixaban or warfarin, with target international normalized ratio 2–3. Echocardiography was repeated at weeks 6 and 12 to assess the LVT size. The percentage of reduction or total resolution during the first 12 weeks was the primary endpoint. Repeated measure ANCOVA was used to evaluate the differences in left ventricular (LV) thrombus size between treatment groups. Results: Twenty-seven patients were recruited: 14 were treated with apixaban and 13 patients with warfarin. Thirteen patients completed treatment in the apixaban arm with one patient lost to follow-up, and one death observed. In the warfarin arm, nine patients completed the study follow-up, and four died during the follow-up. The mean (standard deviation [SD]) reduction in LV thrombus size in apixaban arm was 65.1% (SD 31.3) versus warfarin arm, 61.5% (SD 44.0) at the 12^th week follow-up (P = 0.816). Safety outcomes were similar with both treatment arms. Conclusions: This pilot study suggests that apixaban may have similar effectiveness and safety to warfarin for LVT resolution.

Background: Heart failure with reduced ejection fraction (HFrEF) is one of the most common cardiac diseases causing hospital admission, with a very high short- and long-term mortality rate. The study aims to assess the short-term mortality rate of acute decompensated HFrEF and its correlation with the baseline characteristics in a Nepalese population. Methods: Patients with acute decompensated HFrEF admitted in the unit were prospectively enrolled in this study and were followed up for 3 months. Patients who died and those who did not die were compared using the Chi-square test for categorical variables and Student's t-test was used for the comparison of continuous variables. Results: A total of 100 patients were included in the study. The mean age of the patient was 60 ± 16.18 years, with 55% of the participants being male. Atrial fibrillation was documented in 17% and 16% had bundle branch block. Idiopathic dilated cardiomyopathy was seen in 56% of the participants and was found to be the most common cause of HFrEF, followed by coronary artery disease (18%). Pleural effusion was present in 17% of the patients, out of which bilateral effusion was more common (8%). Twenty-nine percent of the patients died during the 3 months follow-up period. Dyslipidemia, hypertension, ejection fraction, baseline hemoglobin, and creatinine level were significant predictors for mortality (P < 0.05 for all). Conclusion: Dilated cardiomyopathy was the most common cause of acute decompensated HFrEF in the Nepalese population. A very high 3-month mortality rate (29%) was recorded. The presence of cardiovascular risk factors, reduced ejection fraction, baseline hemoglobin, and creatinine levels were significant predictors of mortality in acute decompensated HFrEF patients.