Chirumamilla, Sri Sai Kaumudi

Introduction: Seasonal, geographic, and socioeconomic factors all influence cardiovascular (CV) mortality. Long-term seasonal trends across United States regions remain insufficiently characterized. Research Question: We evaluated longitudinal trends in CV mortality across seasons in the U.S., stratified by geographic region and degree of urbanisation, from 1999 through 2020. Methods: Data on CV mortality (ICD-10: I00-I99) were extracted from the CDC WONDER database and stratified by season (Winter, Spring, Summer, Fall), U.S. Census region (Northeast, Midwest, South, West), and degree of urbanisation (6-level National Center for Health Statistics classification). Age-adjusted mortality rates (AAMRs) were calculated, and Joinpoint regression was used to estimate annual percent change (APC) and average annual percent change (AAPC) with 95% confidence intervals. Results: From 1999 to 2020, 18.8 million CV deaths were recorded (Table 1). Winter accounted for the highest mortality burden across all regions and urban settings but also showed the greatest improvement of the the 20-year study period, with AAPC reductions most pronounced in the Northeast (–2.83%) and Large Central Metro areas (–2.79%; p < 0.000001 for all trends; Figure 1). Summer and Fall, while associated with fewer deaths, showed slower progress, particularly in the Midwest (Fall AAPC: –1.81%; Summer: –1.77%) and rural areas (NonMetro Fall AAPC: –1.56%). Notably, Midwest Fall mortality demonstrated a statistically significant reversal, with an APC increase of +3.87% from 2018 to 2020 (p = 0.02)(Figure 1). Conclusion: CV mortality in the U.S. follows a distinct and evolving seasonal pattern. Although winter remains the deadliest season, it has seen the most substantial mortality reductions, likely tied to improved awareness, continuity of care, and cold-weather adaptations. However, slower progress during summer and fall, particularly in the Midwest and rural areas, reveals growing seasonal and geographic disparities. Most notably, the recent and statistically significant rise in Midwest fall mortality signals an urgent concern. This reversal may reflect emerging climate stressors such as prolonged heat, air pollution, and environmental volatility during transitional months compounded by reduced healthcare access or changing behavioral risk factors. These findings call for year-round, seasonally tailored public health strategies especially for underserved and climate-vulnerable populations.

Abstract Background Catheter ablation for atrial fibrillation (AF) improves quality of life and lowers cardiovascular adverse events. However, AF recurrence rates remain high - thus the need for better or improved predictors of AF recurrence. The role of left atrial (LA) stiffness remains unclear, as prior findings were controversial. Purpose To explore the relationship between a noninvasive LA stiffness index (LAstiffn) and AF recurrence after catheter ablation. Methods We analyzed a prospectively recruited cohort of patients who underwent catheter ablation for AF, were in sinus rhythm at 3 months post-ablation, had no significant (&lt; moderate) valvular disease, and had LA volumes and LA diastolic function prospectively measured. LAStiffn was calculated as (E/e’)/LA emptying fraction (LAEF) ratio (abnormal defined as &gt;15/45≈0.3). Outcome endpoint was the first documented AF/atrial flutter episode, lasting &gt;30s, beyond 3 months post ablation (end of blanking period). Results A total of 589 patients were studied (mean age 60±10 years; 75% men; 50% with persistent AF; Table 1). At 3 months post-ablation, mean LAVI(Left atrial volume index) was 36±10 mL/m2 and LAstiffn 0.32±0.22. LAstiffn tended to be higher in older patients, in females, and patients with persistent AF and comorbidities (hypertension, congestive heart failure, coronary artery disease, CHA2DS2-VASc score ≥2, etc). At multivariable regression analysis, LAstiffn correlated with LV size and mass, degree of mitral/tricuspid regurgitation, and right ventricular systolic pressure. At 1 year, 3 years, and 8 years follow up, AF recurred in 118, 191, and 347 patients, respectively. At univariate Cox proportional hazards regression analysis, LAstiffn index &gt;0.3 was significantly associated with AF recurrence at 1 year (log-rank P=.0005), 3 years (P=.0002), and 8 years follow up (P&lt;.0001; Figure). In multivariate analysis including all clinical and laboratory factors with P&lt;.10 in univariate analysis, LAstiffn &gt;0.3 remained an independent factor for AF recurrence only at 3-years (adjusted HR 1.40 [1.03-1.91], P=.03) and 8 years follow up (adjusted HR 1.65 [1.29-2.13], P&lt;.0001) after adjustment for age, sex, type of AF (persistent/paroxysmal), LA volume index (LAVi), obstructive sleep apnea, and prior pacemaker/ICD implantation (best independent factors); P=.14 at 1 year follow up. In ROC analysis, LAstiffn (AUC 0.61, P=.001) performed slightly better than LA deformation LAEF (AUC 0.59, P=.002) or E/e’ (AUC 0.58, P=.03), though with modest sensitivity/specificity (58%/62%). Conclusions LAstiffn may reflect LA myopathy that is likely due to the cumulative effects of comorbidities, diastolic dysfunction, and intrinsic LA tissue remodeling. LA stiffening may be a substrate facilitating redevelopment of AF, thus patients with increased LAstiffn may need more frequent monitoring to prevent/treat AF recurrence earlier.

Description of Case: A 40-year-old woman presented with a 3-month history of dyspnea. A murmur was found on examination. Echocardiography reported moderate mitral stenosis and regurgitation with diffuse thickening and calcification of the anterior mitral leaflet (Fig1.A), thought to be due to rheumatic disease. She had runs of supraventricular tachycardias not controlled with diltiazem. Her dyspnea progressively worsened; transesophageal echocardiography(TEE) showed severe mitral stenosis and mitral regurgitation (mean gradient 18 mmHg; Fig1.B) with a dense CW Doppler (Fig 1.C) and a mass on left atrial free wall. Cardiac MRI revealed diffuse left atrial thickening with delayed enhancement of the left atrium, left atrial appendage, and extending into the right upper and left inferior pulmonary veins. The mass was initially suspected to be a thrombus. She was placed on rivaroxaban and scheduled to undergo mitral valve replacement. When she presented to our emergency department with dizziness she was found to have paroxysmal atrial fibrillation and pulmonary embolism. On admission she had an intermittent opening snap and a 1/6 mid-diastolic rumble with a 2/6 holosystolic murmur at the apex. Work-up for infectious disease and antiphospholipid syndrome was negative. NT-proBNP was mildly elevated. At surgery the mass invaded the mitral valve and the anterior, septal, and superior part of the left atrial lateral wall and could only be partially excised (Fig1.D). Pathology showed high-grade undifferentiated pleomorphic cardiac sarcoma. Discussion: This case highlights the diagnostic challenges associated with primary cardiac tumors masquerading as valvular pathology. The presentation included dyspnea, typical auscultation of mitral stenosis and features of stenosis on echocardiography. Presumptive diagnoses included rheumatic heart disease, calcific degeneration, infective endocarditis, and autoimmune processes; the atrial mass was initially thought to be a thrombus. A thorough, multidisciplinary approach to diagnosis, utilizing multimodality imaging techniques and ultimately tissue biopsy were required to make the correct diagnosis. Maintaining a broad differential when dealing with valvular masses is key, since relying solely on imaging findings may not suffice for definitive tissue diagnosis.