Sleep Apnea Research Articles

Background: Sleep apnea is a major risk factor for ischemic heart disease (IHD), and the two conditions are closely related. Our study aims to examine mortality trends related to IHD from 1999 to 2020, exploring potential contributions of sleep apnea to disparities across demographic and geographic subgroups. Method: Data related to mortality was extracted from CDC WONDER. The analysis of Multiple Cause of Death Files was conducted from 1999 to 2020 to identify fatalities associated with ischemic heart disease and sleep apnea. Crude rates and age-adjusted mortality rates (AAMRs) per 100,000 populations were calculated for variables including age, gender, race, and geographic regions. Joinpoint regression analysis was utilized to evaluate annual percent changes (APCs) and average annual percent changes (AAPCs). Results: Overall, the AAPC for IHD mortality was 9.15% (p<0.0001) from 1999 to 2020, with notable increases noted between 1999 and 2008 (APC=12.62%, 95% CI: 11.05–14.62) and 2018 and 2020 (APC=12.50%, 95% CI: 6.81–15.65). In comparison to females (8.99%, 95% CI: 8.57–9.78), males had a higher AAPC (9.24%, 95% CI: 8.78–9.83). There were clear racial inequalities, with Whites showing steady increases during the study period (AAPC=9.39%, 95% CI: 8.98–9.85) and Black or African Americans having a rapid increase in 2018–2020 (APC=23.54%, 95% CI: 14.05–29.43). Geographically, the Midwest reported the highest AAPC (10.07%, 95% CI: 9.37–11.86). Both AAMR and crude rates reflected these patterns, with crude rates rising from 0.36 in 1999 to 2.34 in 2020, mirroring the increase in AAMR. Older age groups and populations with higher sleep apnea prevalence exhibited elevated mortality burdens. Conclusion: The findings highlight persistent disparities in IHD mortality, potentially exacerbated by sleep apnea. These statistics underscore the growing impact of IHD and emphasize the need for targeted interventions addressing both IHD and sleep apnea to reduce persistent disparities.

Introduction: Sleep disordered breathing (SDB) has been reported as a common comorbidity in heart failure (HF). Historic cohorts did not include patients using SGLT-2 inhibitors or neprilysin inhibitors, which may have an impact on the prevalence of sleep apnea due to improved cardiac function, decreased sympathetic drive, attenuated inflammation or weight loss. Research Question: Assess the prevalence of SDB including central sleep apnea (CSA) in a contemporary stable population of patients diagnosed HFrEF or HFmrEF at a single cardiovascular center in Poland. Methods: Patients ≥50 years old with stable HF, LVEF<50%, NYHA class ≥II, on optimized GDMT HF treatment, and no prior SDB diagnosis prospectively underwent a WatchPAT® home sleep apnea test to screen for SDB. Subjects were classified as not having SDB if the apnea hypopnea index (AHI) using a 4% desaturation rule was <5 events/hour of sleep, mild SDB if 5≤AHI<15, and moderate-to-severe SDB if AHI≥15. Subjects with AHI≥15 were further classified based on the percentage of AHI that was central. Results: The 200 participants had a median [Q1, Q3] age of 68 [61, 75] years, body mass index 28.1 [25.0, 31.4] kg/m 2 , and LVEF 35% [29, 42]. They were primarily male (84%), NYHA class II (97%; 3% class III) and well-treated on GDMT including 97% using 3 or 4 of the recommended drugs. Of the 200 participants, 71.5% (143) had SDB. Further, 39.0% (78) had moderate-to-severe SDB (Figure 1); obstructive sleep apnea (OSA) was the most common type, but about half of the predominantly OSA participants also experienced a meaningful burden of central events. Predominant moderate-to-severe CSA (central AHI≥50% of AHI) was identified in 9.5% (19) of all participants, while another 15.0% (30) had 10-<50% of events being central and 14.5% (29) had mostly obstructive events (<10% central). Examination of only central events revealed 19.5% (39) of participants had central AHI≥5 and 9.0% (18) had central AHI≥15. Conclusions: There is a significant prevalence of SDB, including CSA, in well-managed patients with HFrEF/HFmrEF despite advances in HF treatments that improve autonomic balance and promote weight loss. Treatment of SDB has demonstrated significant improvements in quality of life in patients with either OSA or CSA but continues to be underdiagnosed and undertreated. Therefore, all patients with HF should be questioned for signs and symptoms of SDB followed by appropriate testing and treatment. Registration: NCT06313840

Background: Evaluating nocturnal regulation of cardiac autonomic nervous system (CANS) with frequency-domain heart rate variability (HRV) is relevant, especially in patients with sleep apnea. So far, the association between very low frequency (VLF) of HRV and major adverse cardiovascular and cerebrovascular events (MACCEs) has not been sufficiently elucidated. Aims: We seek to evaluate the impact of VLF of HRV on MACCEs in patients with hypertension. Methods: This prospective study enrolled 2,061 hypertensive patients from 2017–2021 monitored with nocturnal Holter electrocardiography and type III home sleep apnea testing. Nocturnal HRV was defined by the variation in normal-to-normal intervals at night, and evaluated based on frequency-domain spectra, including high frequency (HF) (0.15–0.5 Hz), low frequency (LF) (0.04–0.15 Hz), VLF (0.0033–0.04 Hz), and the LF/HF ratio. Restricted cubic spline analysis via Cox regression was used to explore the prognostic effects of different HRV indices. The cut-off point for VLF was set at 2,566 ms 2 . Stabilized inverse probability weighting (IPW) based on propensity scores was used to balance baseline characteristics between low-VLF (<2566 ms 2 ) and high-VLF groups (≥2566 ms 2 ). Results: Over a median follow-up of 39 months, 1,867 patients aged 58.4±11.2 years (77.4% men) were included in final analysis. MACCEs occurred in 15.3%. Among 4 HRV indices, only VLF showed a stable nonlinear prognostic association. Compared with patients with high-VLF group, the low-VLF group had a 42–47% higher risk of MACCEs compared to the high-VLF group, depending on the cohort (unadjusted or IPW). In obese patients, those with low-VLF vs high-VLF showed an unadjusted HR of 1.55 for MACCEs (95% CI, 1.21–1.99; P =0.001), which persisted after IPW adjustment (HR 1.38 [95% CI, 1.06–1.81]; P =0.016). Similarly, patients with OSA in the low-VLF group (vs high-VLF group) had an increased risk of MACCEs (unadjusted HR 1.56, 95% CI 1.20–2.02, P =0.001; adjusted HR 1.38, 95% CI 1.07–1.77, P =0.013). The ratio of nocturnal-to-baseline VLF had an area under the curve (AUC) of 0.962 in predicting respiratory event-related cardiac cycle changes during short time intervals. Conclusion: Lower nocturnal VLF of HRV may increase the risk of MACCEs in patients with hypertension, particularly those with obesity and sleep apnea. suggesting a pathophysiological mechanism that links cardiovascular events to impaired regulation of cardiopulmonary coupling by the CANS.

Background: Epicardial adipose tissue is associated with prevalent and incident atrial fibrillation (AF). The mechanism for this association has been at least partially attributed to fatty atrial infiltration, or lipomatous metaplasia (LM), of the left atrium (LA). Objective: The purpose of this study was to quantitate the extent of LA LM using contrast enhanced computed tomography (CECT) and to examine its association with intracardiac electrogram characteristics using high density electroanatomic mapping in patients referred for AF ablation. Methods: The retrospective cohort included consecutive patients who underwent CECT and LA high-density mapping (Pentaray, Biosense Webster) prior to AF ablation between January 2021- 2023. Univariable associations were examined using nonparametric tests. The association of bipolar voltage amplitude and mid-LA myocardial CECT image intensity (< 0 Hounsfield units indicative of LM, ADAS 3D software), at each electroanatomic map point, was examined using a mixed effects linear regression model clustered by patient. Results: The cohort consisted of 34 patients with mean age 66.4 ± 9.5 years, BMI of 31.7 ± 9.5 kg/m2, left atrial volume index (LAVI) 38.0 ± 8.1 mL, and EF 51 ±13%. Of all patients, 41% were female, 65% had persistent AF, 74% had hypertension, 41% had coronary disease, 12% had diabetes, 33% had sleep apnea, and 15% had prior stroke or TIA. LM was detected among 53% of patients (95% CI 36-69%), and was unassociated with age, BMI, LAVI, AF type, sex, diabetes, sleep apnea, or hypertension. Bipolar voltage was associated with CECT attenuation (-0.2 mV/ Hounsfield unit, P<0.001), but was unassociated with LM. Conclusions: LA LM was prevalent in a small cohort of patients undergoing AF ablation and was unassociated with traditional risk factors and voltage mapping. Additional studies are warranted to refine the understanding of LM as an atrial myopathy.

Bariatric surgery is primarily performed using minimally invasive techniques. Intraoperative conversion to open is associated with increased complications. This study aimed to provide a contemporary overview of frequency of conversion to open, compare complication rates and determine factors associated with conversion. The MBSAQIP database from 2020 to 2022 was analyzed to identify two cohorts; those who underwent a minimally invasive approach and those who required conversion to open. Patients undergoing primary sleeve gastrectomy (SG), Roux-en-Y gastric bypass (RYGB), biliopancreatic diversion with duodenal switch (BPD-DS) and single anastomosis duodenal-ileal bypass (SADI) were included. Univariate analysis was performed to characterize differences and assess for rate of complications between cohorts. Multivariate logistic regression was performed to determine factors associated with conversion and 30-day serious complications. A total of 524 224 patients were identified of which 181 (0.03%) required conversion to open. Factors associated with increased risk of conversion to open included age, BMI, lower albumin, sleep apnea, undergoing RYBG or BPD-DS (vs. SG) and previous foregut surgery. Patients converted were more likely to have 30-day reoperation, reintervention, or readmission on bivariate analysis. Conversion to open was also an independent predictor of serious complications on multivariate analysis. Conversion to open in bariatric surgery is rare but associated with significant increased risk of postoperative complications. Patients at increased risk may benefit from preoperative risk mitigation, such as those undergoing BPD-DS or RYGB, with sleep apnea, or with a history of previous foregut surgery.

Introduction: GLP1 receptor agonists (GLP1-RA) are increasingly prescribed, with many of their potential benefits elucidated in recent studies. Consequently, GLP1-RAs were recently approved for the treatment of obstructive sleep apnea (OSA). There is a known strong association between OSA and atrial fibrillation (AF), with up to 5% of OSA patients developing AF and as many as 50% of AF patients having OSA. In this retrospective study, we analyze a cohort of patients with OSA prescribed GLP1-RAs and assess their risk of developing AF as compared to OSA patients who were not prescribed GLP1-RAs. Hypothesis: The use of GLP1-RAs will confer a reduced risk of developing AF in OSA patients. Methods: All Icahn Mount Sinai Health System patients were searched using TriNetX from 1/1/2005-5/31/2025. Patients with OSA, BMI >25, and age >18 years were included. Patients who did not meet the inclusion criteria, those with any arrhythmias prior to the index event, those with central sleep apnea, or those with baseline structural heart disease or heart failure were excluded. The control cohort was composed of included patients who were not prescribed a GLP1-RA. The cohorts were propensity matched and balanced for baseline characteristics (i.e. BMI, hypertension, CPAP device use, age, etc.). Statistical analysis was performed via the Cox regression method using the built-in TriNetX calculator. Outcomes are reported as risk ratios (RR) and 95% confidence intervals (CI). Results: A total of 9,370 patients with OSA were included in the analysis (GLP1 n=4,690; no GLP1 n=4,680). Baseline characteristics of the cohorts are reported in Table 1. The median follow-up from diagnosis of OSA for the non-GLP1-RA group was 958 days. The median follow-up for the GLP1-RA group was 491 days, with a median time from diagnosis of OSA to prescription of GLP1-RA of 380 days (total median follow-up from diagnosis of OSA 871 days). There was a significant 50.1% reduction in the risk ratio of developing AF for OSA patients prescribed GLP1-RAs (RR 0.499, 95% CI 0.342-0.728, P = 0.0002) as compared to those who were not (Figure 1). Conclusion: GLP1-RAs may confer a significant protective effect on patients with OSA in reducing the risk of developing AF. Further research, including prospective randomized-controlled trials, is needed to elucidate the mechanism of this effect and to determine whether the effect of GLP1-RAs is in proportion to the effect of weight loss experienced by the patients.

Introduction: Long-term survival following lung transplant surgery (LT) presents an ongoing challenge, with a five-year survival rate of 55%. Furthermore, adverse LT outcomes are linked to a high incidence of cardiac arrhythmias. Although beta-adrenergic suppression (BAS) can be safely initiated in most patients with severe lung disease, current guideline documents indicate that the role of BAS after LT remains unclear. Therefore, the safety and potential benefits of BAS on long-term survival after LT remain to be determined. Methods: All adult patients who underwent LT at the University of Florida between 2016 and 2021 were identified. Their pre- and post-LT medication use, as well as relevant patient characteristics, comorbidities, and follow-up data (including survival), were recorded in a dedicated database. Results: The LT recipients included in this study (N=299) had mean age 60 ± 11 years, 45% were female, mean body mass index was 26 ± 6kg/m2. Available mean follow up was 4.5 ± 1.9 years. BAS medications were used by 85 (28%) patients pre-LT, and by 210 (70%) patients after LT. A significant survival benefit was evident in patients who were already receiving BAS prior to LT and continued its use post-LT (p = 0.03). Those newly initiated on BAS after LT manifested a comparable survival benefit relative to patients not receiving BAS (p = 0.03, Figure). A combined analysis revealed that all patients for whom BAS was prescribed after LT exhibited prolonged survival when compared to patients without BAS (p = 0.008, adjusted in a multivariate analysis for age, sex, history of smoking, renal insufficiency, coronary artery disease, heart failure, hypertension, hyperlipidemia, and sleep apnea). No survival benefit was observed when analyzing other classes of anti-arrhythmic drugs including Amiodarone after LT. Conclusions: In this large, retrospective, single-center study of long-term survival after LT, patients using BAS lived significantly longer, even after accounting for potential confounders. This benefit extended to both patients newly initiated on BAS and those who were using BAS pre-LT and continued it post-LT. Consequently, routine use of BAS should be considered in appropriate LT patients. Future studies are warranted to build upon these findings, particularly to identify and maximize the potential protective pathophysiologic mechanisms.

Introduction: Catheter ablation is an effective strategy for the maintenance of sinus rhythm and enhancement of quality of life in patients with atrial fibrillation (AF). Oral anticoagulants (OAC) are recommended for at least 3 months post-ablation and indefinitely in patients with CHA 2 DS 2 -VASc score ≥2. Research Question: What is the pattern of OAC use from the time of ablation to one year after ablation with respect to CHA 2 DS 2 -VASc score? Methods: Patients with AF who underwent ablation (index date) from Jan 2017 to Oct 2023 were identified from Optum Clinformatics EDM–DoD. The cohort was divided into three groups: CHA 2 DS 2 -VASc 0 (low risk), 1 (intermediate risk), and ≥ 2 (high risk). Additionally, a subgroup with score ≥ 4 (very high-risk) was assessed. Treatment with OACs ( i.e. , direct oral anticoagulants or vitamin K antagonists) was assessed within the 30-day window following the ablation and at 1-year. Results: Patients with CHA 2 DS 2 -VASc scores 0, 1, and ≥ 2 accounted for 2.8%, 7.5%, and 89.7% of the total population, respectively, with the ≥ 4 subgroup accounting for 61.6% of the total. The mean (SD) age was 52 (9), 58 (9), 70 (8), and 72 (7) years with females accounting for 0%, 14%, 42%, and 48% respectively. Many medical conditions were prevalent including hypertension (86%), obesity (45%), heart failure (44%), sleep apnea (41%), chronic kidney disease (25%) and diabetes (21%). For the low-risk group, OAC discontinuation ranged 66.9 to-78.6% at 1-year, and OAC continuation decreased by ~ 4% from 13.5% to 9.3% between 2017 and 2023. For patients in the intermediate risk group, OAC discontinuation was stable (~ 60%) and the continued use of OAC in the 1-year period increased by ~ 3% from 20.1% to 23.5%. For patients in the high-risk group, OAC discontinuation decreased by ~ 2% from 28.6% to 26.5% and the continued use of OAC increased by ~ 6% from 45.2% to 51.4%. For patients in the very high-risk group, OAC discontinuation minimally decreased, and OAC continuation increased by ~5% from 46.3% to 52%. In a stable minority of patients (~10-20%) across all risk groups, OAC was not used at the time of ablation or after. (Figure 1) Conclusion: Patterns of OAC treatment following AF ablation were variable across CHA 2 DS 2 -VASc score subgroups. The discordance between guideline recommendations and clinical practice with respect to post-AF ablation OAC use may have an important impact on cardiovascular outcomes.

Background: Post-COVID syndrome may present with exertional symptoms that are not explained by noninvasive testing. Invasive cardiopulmonary exercise testing (iCPET) can identify unique hemodynamic and metabolic impairments. Case Presentation: A 52-year-old man with prior COVID-19 infection (2020) and obstructive sleep apnea presented with exertional fatigue, dizziness, and presyncope. Routine investigations, including echocardiogram, stress testing, spirometry, and lab examinations were normal. Neurologic workup revealed preserved epidermal nerve fiber density in skin biopsy, normal quantitative sudomotor axon reflex test (QSART), and normal cardiovascular autonomic reflex testing with tilt, without orthostatic intolerance. Given persistent symptoms, he underwent iCPET with right heart catheterization and arterial line placement. At baseline, right atrial pressure (RAP) was 4 mmHg and cardiac index 2.54 L/min/m2. During exercise to 140 watts (91% predicted VO2), RAP fell to 3 mmHg, and cardiac index rose to 7.0 L/min/m2. Stroke volume declined in late stages. Cardiac output reached 77.4% of predicted. Ammonia rose from 21 to 152 µmol/L and lactate from 1.7 to 11 mmol/L. [Fig 1, Fig 2, Fig 3] Breathing reserve was exhausted (-18.2%). Counterpressure maneuvers improved cardiac output and blood pressure. Oxygenation remained normal. Discussion: This case highlights a potential novel mechanism of post-exertional fatigue: exertional hyperammonemia due to impaired ammonia clearance. The patient’s preserved ventilatory and autonomic profiles, alongside a marked rise in ammonia and lactate, suggest a metabolic dysregulation independent of oxygenation or cardiac output capacity. The sustained hyperammonemia may be attributable to delayed urea cycle clearance or excessive gut production by urease-positive bacteria, possibly due to small intestinal bacterial overgrowth (SIBO). While rare, exercise-induced hyperammonemia has been described in disorders of nitrogen metabolism. In our evolving clinical experience, such patients show improvement with empiric rifaximin therapy and are being studied using exhaled nitrogen breath tests for SIBO, although formal data is pending. Conclusion: In a post-COVID patient with normal autonomic and neurologic testing, iCPET revealed preload insufficiency and exertional hyperammonemia likely contributing to post-exertional fatigue. iCPET can uncover functional and metabolic limitations not detected by standard evaluations.

Introduction: Atrial Fibrillation (AF) and Mitral Regurgitation (MR) share a bidirectional association, and AF is highly prevalent among MR patients. Transcatheter Edge to Edge Repair (TEER) for mitral valve (MV) is offered in severely symptomatic patients. The influence of pre-procedural AF on TEER outcomes is poorly defined. Hypothesis: We hypothesized that patients with AF undergoing TEER for MR would have higher rates of hospitalizations and mortality compared to those without a diagnosis of AF. Methods: We performed a retrospective single-center study where we identified 126 patients who underwent TEER for MR between January 2021 and December 2023. We then stratified the patients into two groups based on documented history of AF: No AF (n=53), AF (n=73). We then performed descriptive and comparative analyses of demographics, pre- and post-procedural echocardiographic parameters for 1 year. The primary outcomes were rates of heart failure (HF) hospitalizations and mortality. Results: Mean age in the AF group was higher at 79 years compared to 76.16 years (p=0.0448). AF population also has a significantly higher incidence of hypertension, chronic kidney disease, and obstructive sleep apnea (OSA). Pre-TEER MV mean gradient was higher in the No AF group (3.045 + 1.49 vs 2.43 + 1.46, p = 0.0315). RA Area is higher in the AF group pre-TEER. While at 1 year, LAVI and RA Area were significantly higher in the AF group. HF hospitalization rates were 17% in the no AF group while in the AF group it was 23.3%, p=0.186. Mortality in the AF group was significantly higher at 28.8% compared to 9.4% in the No AF group, with p=0.0076. Conclusion: Our study showed a significant increase in mortality in the AF group despite similar symptomatic and echocardiographic improvements in both cohorts. Although HF hospitalization rates did not differ significantly, the presence of AF is associated with higher mortality in 1 year. Our findings highlight the importance of aggressive AF management and aim to maintain sinus rhythm post-procedure.

Background: Obstructive sleep apnea (OSA) is associated with increased arterial stiffness and adverse cardiovascular outcomes. Structural and load-dependent components reflect stiffening due to age-related changes in the blood vessel wall and from the pressure load on the arterial wall, respectively. The extent to which OSA severity, measured by Apnea Hypopnea Index (AHI) correlates with these distinct components of arterial stiffness remains unclear. Hypothesis: In a multiethnic cohort, AHI exhibits distinct relationships with structural and load-dependent pulse wave velocity (PWV), contributing variably to total PWV independent of conventional cardiovascular risk factors. Methods: Data from 2,033 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) Exam 5 with corresponding MESA Sleep and Carotid Ultrasound Ancillary Studies were analyzed. AHI defined as all apneas&hypopneas with >=3% desaturation or arousals above 5 events/hour was logarithmically transformed for regression analysis. Total, structural, and load-dependent carotid PWV were calculated using participant-specific models. Multivariable linear regression was performed to assess the impact of AHI on Total, structural, and load-dependent PWV. Results: Participants were 69.9 (±9.5) years old and 53.3% Female. Systolic blood pressure (SBP) was 129.6 (±18.9) mmHg. Total Carotid PWV was 7.41 (±2.0) m/s, while structural PWV was 7.37 (±1.9) m/s and load-dependent PWV was 0.04 (±0.42) m/s. Median AHI was 18.3 (IQR: 9.4, 18.3, 33.1) events/hour. In unadjusted models, AHI demonstrated a significant association with load-dependent PWV (β = 0.038, p = 0.027) but not with structural PWV (β = 0.023, p = 0.178). After adjustment for age and sex, AHI was no longer associated with any PWV component (Table 2). Age correlated significantly with both PWV components, while sex significantly affects only load-dependent PWV (β = 0.078, p < 0.001) with no interaction effects. Conclusion: In this large, multiethnic cohort of older adults, AHI demonstrated a significant correlation with load-dependent PWV but was not meaningfully related to structural PWV. The association with load-dependent AHI was no longer present after adjustment for age and sex.

Background: Obstructive sleep apnea (OSA) is frequently found in individuals with hypertension and is a recognized contributor to adverse cardiovascular (CV) outcomes. While Continuous Positive Airway Pressure (CPAP) remains the primary treatment for OSA, emerging alternatives like pharmacologic agents, oral appliances, and ventilatory support are being explored, especially in patients with resistant hypertension or concomitant CV disease. Methods: A systematic review and meta-analysis were conducted, synthesizing data from 10 studies (out of 223 studies) published in last 15 years, sourced from PubMed, Scopus, and Web of Science Eligible studies included adults with coexisting OSA and hypertension who received interventions such as CPAP, surgery, pharmacologic therapy, or behavioral modification. Outcomes assessed included changes in blood pressure (BP), major adverse cardiovascular events (MACE), stroke, heart failure (HF) hospitalization, and cardiovascular biomarkers. Results: Ten studies involving 870 participants met inclusion criteria. CPAP therapy consistently achieved modest reductions in systolic BP (−4.4 to −10 mmHg) and diastolic BP (up to −7 mmHg). The HIPARCO trial demonstrated a −3.1 mmHg decrease in 24-hour mean BP (p = 0.02), while the MORPHEOS trial reported a −10 mmHg office systolic BP reduction (p < 0.001). Long-term CPAP use maintained systolic BP reductions (−8 mmHg; p = 0.01) and improved BP control in resistant hypertension (40.7% vs 20%; p = 0.024). Acetazolamide reduced mean arterial pressure by 7 mmHg (p = 0.015) and significantly improved apnea-hypopnea index (AHI) when combined with CPAP (p = 0.003). Bosentan yielded a non-significant diastolic BP reduction (−3.1 mmHg; p = 0.101). Oral appliances improved AHI but had limited BP effects. Adaptive servo-ventilation (ASV) surpassed CPAP in lowering BNP levels in HF patients (230.4 vs 847.3 pg/mL; p < 0.05).CPAP reduced cerebrovascular events (HR = 3.1; p = 0.041), hypertensive crises (HR = 5.1; p = 0.006), and MACE. Conclusion: CPAP remains effective for BP control and cardiovascular risk reduction in hypertensive patients with OSA. Combination therapies-particularly CPAP with acetazolamide or ASV-may offer enhanced outcomes. Our findings support a tailored, multimodal treatment strategy and highlight the need for further large-scale RCTs evaluating non-CPAP interventions.

Background: Cardiometabolic (CM) conditions are a recognized complication of obesity, although their comparative burden among patients with severe (class III) obesity is less well known. Objective: To characterize the prevalence of CM conditions among US adults as a function of body mass index (BMI, kg/m2). Methods: Nationally representative, cross-sectional data from the 2017–2020 National Health and Nutrition Examination Survey (NHANES), the most recent survey with comprehensive condition coverage, were evaluated to determine the prevalence of CM conditions as a function of BMI. Seven CM conditions were evaluated: type 2 diabetes (T2DM), cardiovascular disease (atherosclerotic disease or heart failure) (CVD), hypertension (HTN), dyslipidemia (DLP), metabolic syndrome (MetS), metabolic dysfunction-associated steatotic liver disease (LD, including metabolic dysfunction-associated steatohepatitis, fibrosis, and cirrhosis), and obstructive sleep apnea (OSA). Patients were categorized by BMI as normal weight (18.5–24.9), overweight (25.0–29.9), obesity class I (30.0–34.9), obesity class II (35.0–39.9), and obesity class III (40.0 and higher). Population-representative prevalence estimates were derived using NHANES sampling weights and distributions were evaluated with χ 2 tests. Results: In the NHANES weighted sample (n=162,031,595) mean age was 47.7 years, with 50.3% male and 35.1% non-white or Hispanic. The burden of CM conditions was greatest among patients with class III obesity (Table). The prevalence of CM conditions increased in a near-linear fashion across BMI groups, ranging from 0.9 mean total conditions among normal weight adults to 3.3 among those with class III obesity. Conclusion: The burden of CM conditions increases with severity of obesity and is greatest among patients with class III obesity, with patients experiencing an average of 3.3 conditions. Lowering BMI via obesity reduction efforts including anti-obesity medications may attenuate the CM burden associated with obesity.

Introduction: Constrictive pericarditis (CP) is a rare but reversible cause of diastolic heart failure caused by chronic pericardial inflammation, fibrosis, and calcification that impairs ventricular filling. Often misdiagnosed as HFpEF (heart failure with preserved ejection fraction), CP has an estimated U.S. prevalence of 9–10 cases per million. Early recognition is crucial, as surgical pericardiectomy can be curative. Case Presentation: A 60-year-old male with hypertension, type 2 diabetes, and obstructive sleep apnea presented with progressive exertional dyspnea, fatigue, bilateral lower extremity edema, intermittent exertional chest pain, orthostatic dizziness, and palpitations. Initial evaluation in 2022 showed preserved left ventricular ejection fraction and no pericardial abnormalities on transthoracic echocardiogram. Myocardial perfusion SPECT revealed a mild right coronary artery perfusion defect. EKG showed right bundle branch block with nonspecific ST-T changes. In February 2024, left heart catheterization revealed mild coronary artery disease and incidental pericardial calcifications. By June 2024, CT angiography confirmed diffuse pericardial thickening and dense calcifications around the left ventricular apex, consistent with prior pericarditis. Right heart catheterization in July 2024 demonstrated equalization of diastolic pressures (Right Atrium: 25 mmHg, Right Ventricular End Diastolic Pressure: 24 mmHg, Pulmonary Capillary Wedge Pressure: 24 mmHg, Left Ventricular End Diastolic Pressure: 24–25 mmHg), reduced cardiac output (1.6 L/min), low cardiac index (1.7 L/min/m 2 ), and mildly elevated Pulmonary Vascular Resistance (3.2 Wood units), confirming CP. The patient underwent pericardiectomy without cardiopulmonary bypass in August 2024. Pathology showed pericardial calcifications and chronic inflammation. Postoperatively, the patient reported improved exercise tolerance and resolution of symptoms. Discussion: This case highlights the diagnostic challenge of CP, especially in patients without classic risk factors such as prior surgery, radiation, or tuberculosis. The clinical picture mimicked HFpEF, but subtle clues—pericardial calcification and invasive hemodynamic findings—were critical for diagnosis. Timely pericardiectomy led to significant clinical improvement, emphasizing the importance of early recognition and intervention in CP.

Background: Obstructive sleep apnea (OSA) affects about 25% of middle-aged adults and more than doubles cardiovascular disease (CVD) mortality via sympathetic activation, oxidative stress, and metabolic derangements. Clinical risk stratification still relies almost solely on the Apnea-Hypopnea Index (AHI), overlooking heterogeneity in multimorbidity and therapeutic response. Hypothesis: To test whether an unsupervised machine learning pipeline can reveal stable, clinically distinct OSA-CVD phenotypes with different comorbidity burdens and temporal trajectories. Methods: The Wisconsin Sleep Cohort provided 2,570 polysomnographic assessments from 1,123 adults across up to five visits. A two-stage workflow was applied. Stage one used Ward linkage clustering on z-standardized variables, trained an extreme-gradient-boosted tree to rank predictor importance and repeated clustering until fifteen high-yield predictors remained. Stage two reclustered the reduced dataset to assign final labels. Five-fold cross-validation assessed reproducibility. Comorbidity patterns were contrasted, and first-order Markov chains generated transition matrices describing stability. Results: Unsupervised clustering produced four reproducible phenotypes with cross-validated accuracy at 0.82 and adjusted Rand at 0.96. The healthy sleeper group (mean AHI = 6.9 events/h) showed only 2.7% prevalent CVD, whereas the severe OSA (AHI = 52) presented 20.3% CVD. Two mild-OSA groups shared a mean AHI around 11 but differed metabolically: the metabolically healthy phenotype had 4.8% diabetes and 16.5% CVD, while the metabolically healthy phenotype had 54.5% diabetes and 20.7% CVD. Markov modeling revealed strong year-to-year stability for all phenotypes except the severe OSA group, from which 44% of participants migrated to the metabolically unhealthy pattern. Smaller bidirectional flows (10–15%) between the two mild phenotypes suggest gradual, reversible cardiometabolic drift. Conclusions: A data-driven unsupervised framework delineated four reproducible OSA-CVD phenotypes and mapped their temporal evolution. Integrating these phenotypes into routine care may enable proactive surveillance and personalized intervention that lower CVD morbidity among adults with OSA.

Background: Obstructive sleep apnea (OSA) has been linked to increased cardiovascular risk, potentially contributing to adverse cardiac remodeling and arrhythmias through inflammation. However, its specific role in adverse cardicac remodeling and post-operative atrial fibrillation (POAF) in patients undergoing cardiac surgery remains understudied. Hypothesis: We hypothesized that OSA would be associated with adverse structural remodeling, elevated systemic inflammation, and a higher incidence of POAF in patients undergoing cardiac surgery. Methods: Sixty-five cardiac surgery patients (mean age 66 ± 8 years; 25% female) were included, with 13 having OSA and 52 without. Preoperative transthoracic echocardiography assessed cardiac structure and function, including left ventricular (LV) mass, wall thickness, and ejection fraction. Plasma proteomics using Olink proximity extension assays targeted inflammatory markers. POAF was defined as new-onset atrial fibrillation during hospitalization. Statistical comparisons used t-tests and chi-squared tests. Results: OSA and control groups were similar in age (66 ± 7 vs. 66 ± 9 years) and sex (15% vs. 27% female, p= 0.5). OSA patients had higher BMI (32.3 ± 5.2 vs. 28.9 ± 4.6 kg/m 2 , p= 0.035) and showed signs of adverse structural remodeling: increased interventricular septal thickness (1.17 ± 0.21 vs. 1.02 ± 0.21 cm, p= 0.017), posterior wall thickness (1.10 ± 0.19 vs. 0.99 ± 0.16 cm, p= 0.024), and LV mass (114 ± 27 vs. 90 ± 27 g, p= 0.005). Unexpectedly, POAF incidence was significantly lower in OSA patients (7.7% vs. 42%, p= 0.023). Proteomic profiling revealed no significant elevations in canonical inflammatory markers. In fact, CCL25 (8.30 ± 0.60 vs 7.91 ± 0.85, p= 0.0322) and hepatocyte growth factor (HGF) (13.08 ± 0.34 vs 12.93 ± 0.31, p= 0.0244) levels were significantly lower in the OSA group. Conclusions: OSA was associated with increased LV wall thickness and mass, consistent with adverse structural remodeling. Notably, these changes occurred without evidence of elevated systemic inflammation or an increased risk of POAF in our surgical cohort. These findings challenge the presumed link between OSA, inflammation, and post-operative atrial arrhythmias. They suggest that, at least in some surgical populations, OSA may not be accompanied by heightened inflammatory signaling. Further studies in larger and more diverse cohorts are warranted to better understand these complex relationships.

Background: In the United States, Cardiovascular Disease (CVD) is a leading cause of mortality, particularly among individuals with sleep disorders. This national analysis (1999–2020) identifies racial, ethnic, and demographic disparities by analyzing mortality patterns to guide targeted interventions. Aim: To analyze mortality trends in cardiovascular diseases among U.S. adults with sleep disorders, considering socio-demographic variables. Methods: A retrospective analysis was conducted using the CDC WONDER database death certificates from 1999 to 2020 to assess mortality related to CVD in people with sleep disorders for individuals aged 15 to 85+. The population was identified through the International Classification of Diseases, Tenth Revision (ICD-10) codes: I00–I99 for cardiovascular diseases and G47 for the spectrum of sleep disorders. Age-adjusted mortality rates (AAMRs) per 100,000 persons were analyzed and stratified by year, sex, race, census region, and 10-year age group-based classification. AAMR trends across the years were assessed using Joinpoint regression (Version 5.4.0, National Cancer Institute) to determine the annual percent change (APC) and the average annual percent change (AAPC). Results: Between 1999 and 2020, a total of 195,408 cardiovascular diseases (CVD)–related deaths were recorded, with an overall trend showing an increase in age-adjusted mortality rates (AAMRs) from 1.02 per 100,000 in 1999 to 6.87 in 2020, exhibiting consistent fluctuations over the study period. Males consistently demonstrated higher AAMRs compared to females (Females: 4.42 in 2020; Males: 9.92 in 2020). Stratification by race and region showed that Non-Hispanic Black individuals had the highest AAMR, with the trend surging in 2018–2020 (APC: 20.66), while the Midwest recorded the highest rates among all census regions. Ten-year age group stratification indicated that individuals aged ≥85 years had the highest crude mortality rates, contributing disproportionately to the overall national trend. Conclusion: Our analysis reveals a consistent increase in cardiovascular mortality among U.S. adults with sleep disorders, especially in obstructive sleep apnea, with an emerging trend in narcolepsy. Pronounced disparities by race and region were observed. These findings necessitate targeted public health interventions addressing sleep health and cardiovascular risks, to reduce mortality and alleviate the debilitating effects of this association.

Background: Rhythm control with catheter ablation (CA) of atrial fibrillation (AF) leads to reverse remodeling of AF substrate. Comorbidities may impact this process and outcomes. Sparse cardiovascular (CV) guidelines address comorbidities and rhythm control practices after CA. We characterized incident comorbidities after index CA that may impact outcomes, reablation, or antiarrhythmic drug (AAD) practices after CA in the ARRC-AF study. Methods: 2,429,863 patients in Optum’s deidentified Market Clarity Data (Market Clarity ® ) newly diagnosed with AF (2007–2021) were followed until disenrollment, death, or study end; 23,323 patients underwent index CA. Comorbidity status before CA and comorbidity event rates after CA were analyzed. We examined these before and during intervening periods between CAs and while receiving medical therapy. Results: Among the 23,323 patients who underwent index CA (median follow-up: 3.2 years; 44.6% prescribed AADs), baseline comorbidities included hypertension (51.8%), coronary artery disease (17.9%), obstructive sleep apnea (14.4%), diabetes (11.7%), heart failure (10.5%), chronic obstructive pulmonary disease (8.9%), peripheral vascular disease (5.4%), valvular heart disease (4.9%), and chronic kidney disease (1.1%). During follow up, 19,461 patients (83.4%) had no further CA; 3,862 patients (46.7% prescribed AADs) had ≥1 reablation (1 reablation, 14.2%; 2 reablations, 2.0%; ≥3 reablations, 0.4%; interval between Cas of 539, 536, and 458 days, respectively). Individual comorbidity event rates after CA ranged from 0 to 4.7% in the 3 cohorts with ≥1 comorbidity/patient ( Table ). Conclusion: After CA, new comorbidities continue to emerge at a modest rate. In general, comorbidity event rates increased as the number of reablations increased. Both CV and non-CV comorbidities need to be assessed before reablation (with and without long-term AAD therapy) for potential impact on endpoints and need best practice management. Co-morbidities can impact outcomes and need to be considered for their impact on sample sizes, study endpoints, morbidity, and mortality in AF ablation trials. Optimizing management of comorbidities could potentially improve results of AF interventions

Introduction: People living with Human Immunodeficiency Virus (HIV) have increased cardiovascular disease (CVD) risk, yet the specific contributions of antiretroviral therapy (ART) and immune parameters to CVD phenotypes in marginalized populations are underexplored. Research Question: This study examined associations between HIV-specific characteristics (e.g., ART regimen, immunologic markers) and traditional cardiovascular risk factors with CVD outcomes, such as coronary artery disease (CAD) progression, myocardial infarction (MI), and in-stent restenosis (ISR). Methods: A retrospective analysis was performed using electronic health records from individuals with HIV who underwent coronary angiography between 2014 and 2024 at a Houston safety-net hospital. Data included HIV-related factors, demographic, comorbid, and behavioral variables, and CVD outcomes (ejection fraction, MI, ISR, CAD progression - defined as new obstructive lesions or ISR on follow-up angiography). Multivariable logistic regression identified independent predictors, adjusting for relevant confounders. Results: The cohort included 166 individuals (mean age 55 ± 10 years; 78.9% male; 52.4% Black, 24.1% Hispanic, 16.3% White, 7.2% other). A CD4 nadir ≤200 cells/µL was observed in 54.2%, and 35.5% had detectable viral load. Among 122 patients with follow-up angiography, 36 (29.5%) experienced CAD progression. After adjustment, tenofovir use was associated with decreased CAD progression (aOR 0.14, 95% CI 0.03–0.69, p<0.05), while raltegravir (aOR 49.40, CI 1.84–1326.57, p<0.05), cobicistat (aOR 23.57, CI 1.31–425.58, p<0.05), cocaine use (aOR 13.52, CI 2.09–87.60, p<0.01), male sex (aOR 8.55, CI 1.24–59.12, p<0.05), and obstructive sleep apnea (aOR 25.23, CI 2.15–296.64, p<0.05) were associated with increased risk. Higher CD4 count (per 100 cells/µL) was associated with reduced MI risk (aOR 0.74, CI 0.62–0.89, p<0.01). Darunavir use was associated with increased risk of reduced ejection fraction (aOR 12.30, CI 2.35–64.40, p<0.01), and cobicistat with increased ISR (aOR 23.61, CI 1.92–290.94, p<0.05). Conclusion: Specific ART agents and CD4 count were independently associated with distinct CVD outcomes alongside traditional cardiovascular risk factors in this cohort. These insights support considering individual ART and immune status for tailored CVD risk assessment in vulnerable populations with HIV.

Description of Case: A 58-year-old male with history of primary hypogonadism on testosterone replacement therapy, coronary artery disease with prior myocardial infarction, type 2 diabetes, hypertension, hyperlipidemia, obesity, and obstructive sleep apnea on home CPAP presented with typical anginal chest pain. EKG was consistent with inferior STEMI. He was taken for emergent coronary angiography, revealing the culprit lesion: 100% occlusion of the left circumflex coronary artery (LCx) with TIMI 1 flow. Percutaneous Coronary Intervention (PCI) was performed with placement of two drug-eluting stents, and he was given loading doses of dual antiplatelet therapy. There was significant thrombus present requiring manual aspiration thrombectomy, with intravascular ultrasound confirming underlying atherosclerosis. Ultimately, TIMI 3 flow was achieved. Post-PCI, the patient had significant anginal chest pain refractory to medical management. EKG demonstrated resolution of ST elevations, and echocardiogram showed moderately reduced ejection fraction without pericardial effusion or structural complications. His initial hemoglobin was 23.1 (hematocrit 65%), and testosterone levels were markedly elevated above 1,500. We suspected coronary thrombosis may have been partially driven by hyper viscosity from polycythemia, so we performed three therapeutic phlebotomy treatments of 500mL each and gave three one-liter intravenous fluid boluses, until hemoglobin levels were below 18. His chest pain improved markedly after phlebotomy, and he was discharged with close cardiology and endocrinology follow-up. JAK2 mutation test was negative, and testosterone supplementation was discontinued for the interim. Discussion: Only observational data exists thus far, but testosterone-induced polycythemia has been noted as a risk factor for major adverse cardiac events (MACE) in men on testosterone therapy with hematocrit>52% compared to those on therapy with hematocrit<52% 1 . Moreover, any degree of polycythemia is associated with increased MACE as early as 3 months after testosterone initiation 2 . Phlebotomy is mainstay treatment for JAK2-positive polycythemia, targeting hematocrit<45% to reduce MACE 3 . This case demonstrates how ACS in the setting of polycythemia may present with a thrombotic phenotype in younger patients. Furthermore, post-PCI chest pain may be alleviated with therapeutic phlebotomy when hematocrit is dangerously high, regardless of JAK2 positivity.