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PurposeCardiac rehabilitation (CR) improves clinical outcomes in patients with cardiovascular disease (CDV). Patients with CVD often have multiple comorbidities, including obstructive sleep apnea (OSA), potentially affecting their ability to participate and achieve functional improvement during CR. We aimed to test the hypothesis that OSA reduces peak exercise capacity (EC) in patients undergoing CR and to explore if OSA treatment modifies this relationship.MethodsData from a retrospective cohort of CR patients was analyzed. OSA was defined as a respiratory event index > 5/h or physician diagnosis. Patients with OSA were considered "treated" if using continuous positive airway pressure regularly during the CR period. Change in METs was the primary study outcome.ResultsAmong 312 CR patients, median age of 67 years, 103 (33%) had known OSA (30 treated, 73 untreated). Patients with OSA vs. those with no OSA were more likely to be obese and male; otherwise, groups were similar. Compared with the no OSA group, patients with OSA had lower pre-CR METs (3.3 [2.9-4.5] vs. 3.9 [3.1-5], P = .01) and lower post-CR METs (5.3 [4-7] vs. 6 [4.6-7.6], P = .04), but achieved a similar increase in METs post-CR (1.8 [0.6-2.6] vs. 2.0 [0.9-3], P = .22). Furthermore, compared to no OSA, pre-CR and post-CR METs tended to be similar in patients with treated OSA, but lower in untreated patients, with similar increases in METs across all groups, even when adjusting for covariates via multivariable regression.ConclusionOSA is prevalent in patients with CVD undergoing CR. CR substantially improves exercise capacity independent of OSA status, but screening for-and treatment of-OSA may improve the absolute exercise capacity achieved through CR.

Background: Diabetic cardiomyopathy (DbCM) is characterized by asymptomatic stage B heart failure (SBHF) caused by diabetes-related metabolic alterations. DbCM is associated with an increased risk of progression to overt heart failure (HF). The prevalence of DbCM in patients with type 2 diabetes (T2D) is not well established. This study aims to determine prevalence of DbCM in adult T2D patients in real-world clinical practice., Methods: Retrospective multi-step review of electronic medical records of patients with the diagnosis of T2D who had echocardiogram at UC San Diego Medical Center (UCSD) within 2010-2019 was conducted to identify T2D patients with SBHF. We defined "pure" DbCM when SBHF is associated solely with T2D and "mixed" SBHF when other medical conditions can contribute to SBHF. "Pure" DbCM was diagnosed in T2D patients with echocardiographic demonstration of SBHF defined as left atrial (LA) enlargement (LAE), as evidenced by LA volume index ≥ 34 mL/m 2 , in the presence of left ventricular ejection fraction (LVEF) ≥ 45%, while excluding overt HF and comorbidities that can contribute to SBHF., Results: Of 778,314 UCSD patients in 2010-2019, 45,600 (5.9%) had T2D diagnosis. In this group, 15,182 T2D patients (33.3%) had echocardiogram and, among them, 13,680 (90.1%) had LVEF ≥ 45%. Out of 13,680 patients, 4,790 patients had LAE. Of them, 1,070 patients were excluded due to incomplete data and/or a lack of confirmed T2D according to the American Diabetes Association recommendations. Thus, 3,720 T2D patients with LVEF ≥ 45% and LAE were identified, regardless of HF symptoms. In this group, 1,604 patients (43.1%) had overt HF and were excluded. Thus, 2,116 T2D patients (56.9% of T2D patients with LVEF ≥ 45% and LAE) with asymptomatic SBHF were identified. Out of them, 1,773 patients (83.8%) were diagnosed with "mixed" SBHF due to comorbidities such as hypertension (58%), coronary artery disease (36%), and valvular heart disease (17%). Finally, 343 patients met the diagnostic criteria of "pure" DbCM, which represents 16.2% of T2D patients with SBHF, i.e., at least 2.9% of the entire T2D population in this study., Conclusions: Our findings provide insights into prevalence of DbCM in real-world clinical practice and indicate that DbCM affects a significant portion of T2D patients., (© 2024. The Author(s).)

Purpose: Obstructive sleep apnea (OSA)-related pulmonary hypertension (PH) can often be reversed with treatment of OSA via continuous positive airway pressure. We hypothesized that treatment of OSA would be associated with a greater improvement in exercise capacity (EC) with cardiac rehabilitation (CR), especially in patients with PH as compared with those who are untreated., Methods: We reviewed medical records of 315 consecutive patients who participated in CR. Pulmonary hypertension status was assessed on the basis of peak tricuspid regurgitant velocity (>2.8 m/sec) on pre-CR echocardiograms. The OSA status (no, untreated, or treated OSA) was determined on the basis of results from sleep studies, continuous positive airway pressure device data, and physician notes. Exercise capacity was assessed by measuring metabolic equivalents (METs) using a treadmill stress test before and after CR., Results: We included 290 patients who participated in CR with available echocardiographic data: 44 (15%) had PH, and 102 (35%) had known OSA (30 treated and 72 untreated). Patients with OSA versus those with no OSA were more likely to have PH ( P = .06). Patients with PH versus no-PH were associated with significantly lower baseline METs in crude and adjusted analyses ( P ≤. 004). The PH and OSA status in isolation were not associated with changes in METs ( P > .2) with CR. There was a significant interaction between OSA treatment and PH in crude and adjusted analyses ( P ≤.01): treatment vs no treatment of OSA was associated with a clinically and statistically greater improvement in METs in patients who participated in CR with but not without PH., Conclusion: Baseline PH was associated with decreased baseline EC but did not attenuate CR-related improvements in METs. However, in the subset of OSA patients with PH, OSA therapy was associated with improved EC after CR., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Despite differing underlying pathophysiology, type 1 and type 2 myocardial infarction share many of the same diagnostic criteria and can be challenging to differentiate in clinical practice. Correctly differentiating type 1 from type 2 myocardial infarction is important because they are managed differently. The aim of this study was to compare the patterns of rise of cardiac troponin (cTn) and creatine kinase MB (CK-MB) in type 1 and type 2 myocardial infarction., Methods: We analyzed retrospective data on 200 patients with myocardial infarction (97 with type 1, 103 with type 2), excluding patients with ST-segment elevation myocardial infarction. The percentage rise from trough to peak values and the ratio of the peak to the upper limit of normal (RULN) were calculated for both cardiac troponin T (cTnT) and CK-MB. The ratio of peak cTnT to peak CK-MB was also calculated before and after adjusting for sex, glomerular filtration rate (GFR), and infarct size., Results: Type 1 myocardial infarction tended to be larger than type 2 myocardial infarction, with a significantly higher mean percentage rise for both cTnT and CK-MB as well as higher mean RULN (207 vs 86 for cTnT, P = 0.02; 9 vs 4 for CK-MB, P = 0.002). There was a trend toward a higher rise of cTnT than CK-MB in type 2 compared with type 1 myocardial infarction, as demonstrated by the ratio of peak cTnT to peak CK-MB (0.09 in type 2 myocardial infarction vs 0.06 in type 1 myocardial infarction, P = 0.06). This difference persisted after adjusting for sex, GFR, and infarct size (P = 0.05)., Conclusion: Both cTnT and CK-MB rise higher in type 1 than in type 2 myocardial infarction. Meanwhile, cTnT tends to rise out of proportion to CK-MB in type 2 myocardial infarction. These patterns may have considerable implications for the differentiation and subsequent treatment of patients with type 1 versus type 2 myocardial infarction., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Postural orthostatic tachycardia syndrome (POTS) is a debilitating disease that predominantly affects young women. It is a multifactorial disorder that is characterized by severe tachycardia and orthostatic intolerance. Patients with POTS experience a variety of cardiac, neurological, and immunological symptoms that significantly reduce quality of life. In this review, a comprehensive framework is provided to aid in helping identify and treat patients with POTS. Given its heterogenous nature, it is crucial to understand each component of POTS in relation to one another instead of distinct parts. The framework highlights the overlap among the five main subtypes of POTS based on its pathophysiology (neuropathic, hypovolemic, primary hyperadrenergic, joint-hypermobility-related, and immune-related). Emphasis is placed on incorporating a multidisciplinary approach when treating patients with POTS, especially with a new focus towards immunotherapy. Although research has advanced our knowledge of POTS, there is still a critically unmet need to further our understanding and provide patients with the relief they need.

Acute myocardial infarction (MI) provokes a systemic inflammatory response that may contribute to the development of left ventricular systolic dysfunction (LVSD) and heart failure (HF). Patients with post-infarct HF with concomitant LVSD have the most unfavourable long-term prognosis. Measurement of C-reactive protein (CRP) concentration reflecting an involvement of inflammatory pathways in post-infarct myocardial damage offers an attractive strategy to improve risk stratification and clinical decision-making for early management of high-risk patients. Despite growing evidence for the prognostic value of CRP both as a single factor and as a component of multi-marker approach in MI, CRP measurement is not yet incorporated into current guidelines. This may be due to conflicting results reported in existing studies related to various limitations in study designs, such as retrospective case control design, prior myocardial damage, CRP measurement with low-sensitivity assays, non-homogenous populations with acute coronary syndromes, different treatment strategies, small sample sizes, and the lack of left ventricular ejection fraction assessment and long-term clinical and echocardiographic monitoring. As a result, previous studies have not provided conclusive evidence of the prognostic value of CRP for post-infarct LVSD or HF. Future studies with an adequate design including upstream mediators of inflammation as inflammatory markers are needed to identify the best biomarker-based strategies for identifying high-risk patients. Further clinical trials involving anti-inflammatory therapies target-ing different pathways of inflammatory activation in MI should test the inflammatory hypothesis of post-infarct LVSD and HF. Identifying high-risk patients with persistent post-infarct inflammatory response may allow incorporation of pathophysiological guidance for implementation of personalised treatment approaches.