MaxCure Hospitals

Background: Hypertension (HTN) is the primary modifiable risk factor for chronic coronary syndrome (CCS), which significantly contributes to morbidity and mortality. This study aimed to gather expert consensus from Indian cardiologists on managing HTN in patients with CCS, to optimize therapy and improve patient care. Methods: A consensus is based on Indian cardiologists’ inputs collected via an online survey. The questionnaire covered diagnostic practices, clinical patterns, and real-world treatment regimens for managing hypertensive CCS patients. Survey responses were analyzed and discussed during round table meetings. Further expert opinions were graded from Level A (strong consensus) to Level D (no consensus). Recommendations were formulated based on collective expert opinions. Results: The consensus highlights the clinical strategies for managing patients with CCS and associated comorbid conditions. The key diagnostic tools, such as ambulatory blood pressure monitoring and Holter electrocardiogram, are strongly recommended for comprehensive evaluation. Pharmacological management should prioritize the use of angiotensin II receptor blockers and beta-blockers combinations, particularly telmisartan–metoprolol fixed-dose combination (FDC) in the management of hypertensive CCS patients with type 2 diabetes mellitus or dyslipidemia. Conclusions: Indian cardiologists emphasized the importance of using, telmisartan–metoprolol FDC as a preferred drug regimen owing to their cost-effectiveness, improved efficacy, and enhanced adherence. These consensus recommendations aim to enhance therapeutic outcomes and guide future clinical practice in Indian context.

Bradyarrhythmia is a common and potentially serious cause of syncope, often difficult to detect due to its intermittent nature. Traditional ECG monitoring methods either provide low diagnostic accuracy or delay diagnosis, increasing the risk of recurrence. We hypothesized that a deep learning-enabled, 24-hour, single-lead ECG could detect past episodes of bradyarrhythmia. Using unselected 14-day single-lead ambulatory ECG recordings, we developed a deep learning model to identify patients with prior asystole from sinus arrest or complete heart block. The model was trained using the last 24 hours of each recording, free of bradyarrhythmias, to identify daytime sinus pause of ≥3 s, anytime sinus pause of ≥6 s, complete heart block, or a composite of these bradyarrhythmias from the previous 13 days. A total of 320 959 unselected 14-day ambulatory ECG recordings (mean age, 60.5±17.8 years; 60% female) were split into training (n=189 414), tuning (n=45 982), internal validation (n=43 390), and external validation (n=42 173) sets. External validation of prior daytime sinus pause ≥3 s, anytime sinus pause ≥6 s, complete heart block, and a composite end point demonstrated an area under the receiver operating characteristic curve of 0.89, 0.87, 0.93, and 0.89, respectively, with negative predictive values between 97.9 and 99.9%. In addition to this approach of uncovering past events, our model was also tested for its ability to predict bradyarrhythmias within the following 13 days using the first 24 hours of ECG data, achieving an AUC of 0.88 for the composite end point. A deep learning-enabled ambulatory ECG is capable of unmasking underlying conduction tissue system disease. This tool may help identify patients with significant intermittent bradyarrhythmia, potentially improving timely diagnosis and management.

A 35-year-old female presented with heart failure. She was evaluated and found to have persistent left superior vena cava, no right superior vena cava (RSVC), coronary arteriovenous fistula into left-sided superior vena cava (LSVC) with left-to-right (L-R) shunt. She underwent closure of fistula using cardiopulmonary bypass and antegradeandretrograde cardioplegia. After opening the distal left circumflex, a coronary probe was passed through the fistula to delineate the course. The fistula was closed from both ends using a pericardial patch. This is a very rare anomaly with a single SVC.

e15040 Background: Liquid biopsies analyzing circulating tumor DNA (ctDNA) and circulating tumor cells (CTCs) allow minimally invasive monitoring and testing of lung cancer at different stages. It is known that 90% of patients succumb due to metastasis. However, accounting for patients with early metastatic signatures is extremely challenging. In addition, monitoring minimal residual disease (MRD) and identifying patients for recurrence is very prudent. While the role of CTCs in % prediction of survival has been established in several cancers. However, CTC's co-occurrence role with CtDNA and vice versa is not implored in monitoring the aggressiveness of the disease, response to therapies, and therapy decisions. In this study, we investigated ctDNA and CTC's combined roles in monitoring disease aggressiveness and metastasis in lung cancer patients. Methods: A cohort of 265 lung cancer patients with late-stage cancer were retrospectively analyzed for co-occurrence of dual biomarker ctDNA and CTC. The results were correlated as quadrant to assess clinical disease states, obtained from PET scans and HPE findings. Next Generation Sequencing (NGS) test was performed using OncoMonitor dual biomarker assay having CTC enumeration with PD-L1 expression. CTC count was performed using the OncoDiscover Liquid Biopsy Test, approved by CDSCO-India, in 1.5 ml of blood. Results: CTC distribution in this study ranged from 1-8 CTCs with a mean CTC distribution of 1.22. Amongst these patients, 75.47% (n = 200) showed the presence of CTCs and amongst these 200, 91.50% (n = 183) showed PD-L1 expression on their CTCs with a mean value of 0.99. While both biomarkers were positive for ctDNA and CTC (ctDNA+/CTC+) in 135 (50.94%) patients. Interestingly, only 19 (7.17%) patients were negative for both ctDNA and CTC (ctDNA-/CTC-). Similarly, 43 patients (16.23) were positive for ctDNA and negative for CTC (ctDNA+/CTC-), while 68 (25.66%) patients were negative for ctDNA and positive for CTC (ctDNA-/CTC+). The ctDNA+/CTC- cohort had the highest metastatic rate of 62.8%, with ctDNA+/CTC+ at 57.0%. Noteworthy, the ctDNA+ cohort showed the highest % of progressive disease patients with 20.2% and 18.6% along with CTC+ and CTC- status, respectively. The mutations, EGFR, TP53, and KRAS were observed in 62.64% (166/265) of patients. Only stable disease was observed in 29.4% of patients when both biomarkers ctDNA-/CTC- were absent. Conclusions: Overall, the ctDNA+ cohort showed a higher rate of MRD, progression, and metastasis with no stable disease. The quadrant that combined clinical results of the CTC-PD-L1 cells and CtDNA manifest the non-invasive monitoring of disease progression, treatment response, complete remission, and utility of early metastatic detection in lung cancer patients.

The shoulder is the most mobile joint and also the most commonly dislocated joint in our body. Anterior dislocation of the shoulder is more common than posterior and inferior dislocation. Anterior dislocation of the shoulder can be easily reduced by the Stimson technique, traction-counter traction technique, etc. Reducing an acute anteriorly dislocated shoulder is usually easy, but in some instances, it can be difficult due to the interposition of the long head of the biceps, subscapularis, or impacted Hill-Sach. This is a case report of a patient with 10 days old irreducible anterior dislocation of the shoulder. Magnetic resonance imaging (MRI) shows the anterior capsule trapped between the humeral head and glenoid, which does not allow the shoulder to be relocated. This case report highlights the possibility of anterior capsule entrapment in the glenohumeral joint with the subscapularis being intact and that it can be managed by arthroscopy, which has fewer complications than open surgery. A 55-year-old male came with irreducible anterior dislocation of his left shoulder after a slip and fall on his outstretched hand. There was a history of attempts to reduce the dislocation in another hospital but failed to reduce it even under sedation. An MRI of the left shoulder shows that the anterior capsule got entangled between the humeral head and glenoid, as shown in Fig. 1 and 2, and is not allowing the humerus head to reduce. There are reports of the irreducible anterior dislocated shoulder due to interposition of the subscapularis muscle, long head of biceps, greater tuberosity fracture fragment, etc., and are managed by open surgery. In our case report, we managed to disengage the entrapped anterior capsule by arthroscopy after a trial of closed reduction under general anesthesia. Irreducible shoulder dislocation is not a common problem. There are many pathologies that result in the irreducibility of shoulder dislocation; anterior capsule entrapment is one such pathology. Open surgery is not the only solution to address these pathologies; we can treat them by arthroscopy technique, which can address all associated pathologies with minimal complications, unlike open surgery.

DiGeorge syndrome is a congenital primary immunodeficiency disorder resulting from failure of appropriate development of the third and fourth pharyngeal pouches during embryonic phase of development. DiGeorge syndrome usually presents with a clinical triad of immunodeficiency, congenital cardiac defects and hypocalcemia due to hypoparathyroidism. Here, we report a case of DiGeorge syndrome in a neonate with no associated facial dysmorphism and typical phenotype but initially presenting with apnea and suspected septic shock. Subsequent laboratory findings, clinical imaging and molecular genetic testing helped us to reach the diagnosis.

Background Chronic kidney disease (CKD) is characterized by progressive loss of kidney function. Tumor necrosis factor-alpha (TNF-α) is a cytokine implicated in inflammatory processes, including those affecting the kidneys. Although this association is not yet comprehensible, a tie-up between renal disease and markers of inflammation - interleukin-6 (IL-6), preceded by TNF-α - is eminent. However, a pause in research is evident concerning the TNF-α gene with kidney disease in the inhabitants of India. So, this study investigates the association between TNF-α rs1800629 polymorphism and CKD. Methodology A prospective case-control study was conducted in Andhra Pradesh for over three years. A total of 579 patients participated in the study. These were divided into premature, late-stage CKD, and control groups. The amplification refractory mutation system (ARMS)-polymerase chain reaction (PCR)was used, and biochemical investigations and genotyping were carried out for the study participants. Hardy-Weinberg expected frequencies (HWE) with chi-square test was used for detecting allele and genotype frequencies. The association between TNF-α (-308 G/A, rs1800629) and CKD was assessed using odds ratios (ORs) with 95% confidence intervals (CIs). Results We found a higher prevalence of CKD among males (n= 301, 52%) compared to females (n= 278, 48%).Both male and female participants diagnosed with CKD exhibited significantly elevated blood urea and serum creatinine levels compared to the control group, indicating impaired kidney function.Furthermore, these markers were generally higher in the late-stage CKD group compared to the early-stage group, suggesting a progressive decline in kidney function as the disease worsens. The homozygous genotype GG was more prevalent in late-stage CKD patients compared to both early-stage CKD patients and controls. Further, the heterozygous genotype GA was more frequent in the early-stage CKD group compared to the late-stage group.The homozygous genotype AA also showed a higher prevalence in the early-stage CKD group compared to the late-stage group. The G/G genotype and the G allele (rs1800629) were significantly associated with susceptibility to CKD (P<0.005). Conclusions Our study reported the TNF-α rs1800629 polymorphism and CKD risk in a South Indian population. G/G genotype and the G allele (rs1800629) were significantly associated with the risk of CKD. However, further research with larger sample sizes is warranted to confirm these observations and elucidate the underlying mechanisms by which TNF-α might influence CKD risk.