Yinadsawaphan, Thanaboon

Background/Objectives: In the United States, HF prevalence is projected to progressively rise by 2030. Prior research suggests a strong association between reduced sleep duration and increased cardiovascular disease and HF risk. This study introduces an alternative parameter, the weekend sleep recovery (WSR), measured by the weekend-to-weekday sleep duration ratio (SDR), to evaluate its association with HF risk. Methods: We conducted a cross-sectional analysis of NHANES (National Health and Nutrition Examination Survey) 2017–2023 to examine self-reported sleep patterns. Participants were classified as WSR (SDR > 1) or non-WSR (SDR ≤ 1). Multivariate logistic regression assessed the association between WSR and HF, adjusting for demographics and comorbidities. Results: Among 8320 participants included in the fully adjusted analysis, WSR was associated with lower odds of HF compared with non-WSR (adjusted OR 0.73, 95% CI 0.55–0.96; p = 0.026). A significant interaction was observed between WSR and weekday sleep duration (P for interaction = 0.003), whereas no interaction was found with weekend sleep duration. In exploratory subgroup analyses, nominally significant associations were observed in several clinical subgroups; however, after correction for multiple comparisons, only participants without dyslipidemia retained statistical significance. No significant effect modification by race/ethnicity was observed (P for interaction = 0.436). Conclusions: Weekend sleep recovery was associated with lower odds of HF in this cross-sectional study. The association varied according to weekday sleep duration but was generally consistent across racial/ethnic groups. Given the observational design, these findings should be interpreted as associative rather than causal and warrant confirmation in prospective studies.

Spontaneous type-1 Brugada patterns are associated with an elevated risk of major arrhythmic events, yet the relationship between varying degrees of pattern burden and the occurrence of a first major arrhythmic event remains unclear. This retrospective cohort study included 64 adult patients with a spontaneous type-1 Brugada pattern, who were identified at Mayo Clinic sites and followed for ≥12 months after the initial diagnosis. All patients underwent at least three 12-lead electrocardiograms (ECGs) within the first year. Individuals with prior major arrhythmic events were excluded. The percentage of ECGs showing a type-1 pattern was calculated and categorized as paroxysmal (<50%), persistent (50–99%), or permanent (100%). During a median follow-up of 92 months, seven patients (11%) experienced their first major arrhythmic event. Of these, one had paroxysmal, four had persistent, and two had permanent spontaneous type-1 Brugada patterns. Although statistical significance was not reached, the hazard ratios suggested a trend toward increased risk with persistent and permanent patterns compared to paroxysmal patterns. No sudden cardiac deaths occurred during follow-up. These findings suggest that a higher burden of spontaneous type-1 Brugada patterns may be associated with increased arrhythmic risk.

Background: Heavily calcified coronary bifurcation lesions present significant challenges during percutaneous coronary intervention, particularly during atherectomy due to the risk of side branch occlusion from plaque shift. We describe the "Double Guiding Catheter Technique" to minimize side branch closure and wire damage to non-atherectomy vessels during bifurcation orbital atherectomy (OA). Case: A 74-year-old male with a recent NSTEMI presented for elective coronary artery revascularization. A coronary angiogram revealed non-obstructive left coronary arteries and a dominant right coronary artery (RCA) with heavily calcified stenosis at the bifurcation of the right posterolateral (RPL) and right posterior descending (RPD) branches. After placing temporary transvenous pacing and inserting sheaths in the right radial and right femoral arteries, both the RPL and RPD were wired with coronary guidewires. Using a coronary microcatheter, the wire in RPL was replaced with a ViperWire guidewire for OA, while the microcatheter in RPD served as guidewire protection. OA of RPL was successfully performed with the Diamondback 360° OA system (Cardiovascular Systems Inc), followed by multiple dilatations with non-compliant balloons and placement of two drug-eluting stents in the distal RCA to RPL and RPD, achieving good angiographic and IVUS results. Discussion: The Double Guiding Catheter Technique has been described in a few case reports of heavily calcified left main coronary bifurcation atherectomy which is limited to relatively proximal lesions due to the need to pass a second wire to a non-atherectomy vessel outside a guide extension catheter for the main branch. This is the first reported case of OA using this technique in the right coronary artery and a relatively distal part of the coronary artery. The primary advantage of this technique is eliminating the need to withdraw one of the two wires, which can be challenging when recrossing the side branch. The microcatheter can safely protect the other branch wire during atherectomy. Conclusion: By maintaining both wires with a protective microcatheter, OA of coronary bifurcation stenosis can be successfully achieved, potentially reducing the risk of wire transection.

Introduction: Menopause is known to be associated with myocardial infarction (MI). However, the association between menopause age and MI onset in a nationally representative population remains unknown. Objective: To examine the correlation between age of menopause and age of MI onset in the general population and the association between early menopause (onset of menopause ≤ 40 years old) and early onset of MI (onset of MI ≤ 40 years old). Methods: A cross-sectional study was conducted using a population from the 2017-2020 National Health and Nutrition Examination Survey (NHANES). The questionnaire collected self-reported data on the participants' menopause age and their age of first MI. The relationship between these two parameters was analyzed by multivariate linear and logistic regression analyses. Multivariate analysis was adjusted for race, age, body mass index (BMI), smoking status, diabetes mellitus (DM), hypertension, and dyslipidemia status. Results: Among 2,200 postmenopausal females, 90 (4.1%) have had MI. The study involved 85 postmenopausal females who reported both menopause age and MI onset, with a mean ± SD age of 55 ± 13 years. This study found a significant association between menopause age and MI onset. After adjusting for confounders, it was found that every 1-year increase in the age of menopause will delay the onset of MI by 0.28 years, with a 95% CI of 0.013 to 0.552 (Table 1A, Graph 1A, Graph 1B). Additionally, early menopause carries an almost significantly increased risk of 2.11 times (95% CI: 1.00, 4.45) for early-onset MI. After adjusting for confounders, the magnitude of the association was lower and not statistically significant, but the direction remains (OR (95% CI): 2.08 (0.87, 4.95)). However, after stratification with comorbidities, DM status was identified as an effect modifier, with early MI significantly observed in patients with DM in both univariate and multivariate analyses, with OR (95% CI) of 3.03 (1.10, 8.37) and 4.88 (1.26, 18.96), respectively (Table 2A). Conclusion: This study demonstrated a positive association between menopause age and MI onset in a generally representative population. This suggests that prolonged estrogen exposure due to late menopause may delay the onset of MI. Additionally, early menopause was associated with early MI onset in the DM population. Further longitudinal studies are required to examine the potential mechanisms involved in menopause onset and MI onset.

Background: There is suspicion that estrogen may protect against atherosclerosis. Women who experience menarche earlier, and thus have earlier estrogen exposure, might develop atherosclerosis later. The relationship between menarche age and the onset of angina pectoris, a symptom of coronary artery disease, remains unknown. Goal: This study aims to find the correlation between menarche age and the onset age of angina pectoris, and the association between early menarche (onset of menarche ≤ 10 y/o) and early onset of angina pectoris (onset of angina pectoris ≤ 40 y/o). Methods: A cross-sectional study using a population from the 2017-2020 National Health and Nutrition Examination Survey (NHANES). The question collects self-reported data on onset of menarche and onset of angina pectoris. The relationship between menarche age and age in onset of angina pectoris was analyzed by linear and logistic regression analysis. Multivariate analysis adjusted for race, age, body mass index (BMI), smoking , diabetes mellitus (DM), hypertension, and dyslipidemia status. Results: Among 4,816 females who reported their menarche age, 88(1.8 %) have had an angina pectoris. The study involved 82 females who reported both the age of menarche and the age of onset of angina pectoris. The mean ± SD of the age at menarche and the age at onset of angina pectoris was 12.53 ± 1.79 y/o and 51.66 ± 15.16 y/o, respectively. The study found a significant association between the menarche age and the age at onset of angina pectoris. After adjusting for confounders, we found that every 1-year increase in the age of menarche will delay the onset of angina pectoris by 1.43 years, with a 95% CI of 0.01 to 2.86.(Table 1A,Graph 1A-1B) We also found that early menarche has a significantly increased risk 2.8 times (95%CI: 1.3, 6.2) of early onset of angina pectoris.After adjusting for confounders, the association became even stronger. The odds ratio (OR) increased to 3.3 (95%CI: 1.4, 8.0), indicating that women with early menarche were 3.3 times more likely to experience early angina pectoris compared to those with later menarche.(Table 2A) Conclusion: In contrast to our hypothesis, age at menarche is positively associated with onset of angina pectoris. The earlier onset of menarche is linked to the earlier onset of angina pectoris. We suspected that factors beyond estrogen levels may contribute to this unexpected finding. Additional studies are needed to examine the cause of this correlation.

Abstract Background Short sleep is linked to increased acute myocardial infarction (MI) risk.However, the association of weekend-to-weekday sleep patterns with MI in a nationally representative population remains unknown. The goal is to investigate how weekday and weekend sleep durations affect myocardial infarction (MI) in the general population, and if longer weekend sleep can offset insufficient weekday sleep's effects. Methods A cross-sectional study utilized data from the 2017-2020 NHANES to examine the relationship between sleep patterns and MI. Participants self-reported their average sleep durations on weekdays (1) and weekends (2), along with the calculated weekend-to-weekday sleep duration ratio (SDR) (3). Logistic regression models, adjusting for various factors, including demographics and comorbidities, were employed to analyze the association. Those with SDR &gt; 1 had more weekend sleep, while an SDR = 1 indicated equal sleep durations. Results The study involved 9,205 adult participants, with a mean ± SD age of 68.8 ± 10.8 years and 30.7% being female. Among them, 4.65% (428 patients) had a history of MI. The mean ± SD of weekday and weekend sleep hours was 7.6 ± 1.7 and 8.3 ± 1.8 hours, respectively. For weekday sleep duration, after univariate analysis, individuals compared to those in Q1 were statistically significant 0.72 times less likely in Q2 and 1.4 times more likely in Q4 to experience MI . While MI was 0.76 times less likely to occur among participants in Q3, it was not statistically significant (95% CI Q2: 0.54, 0.96; Q4: 1.05, 1.76; Q3:0.57, 1.00). After adjusting, participants only in Q3 were statistically significant 0.71 times less likely to develop MI.(Q3: 95% CI 0.51, 0.99). For weekend sleep duration, the univariate analysis showed that individuals in Q2, Q3, and Q4 were significantly less likely to experience MI (OR = 0.63, 0.67, and 0.69; 95% CIs: 0.48-0.82, 0.51-0.87, 0.53-0.90, respectively) After adjusting, only participants in Q2 were statistically significant less likely to develop MI (OR = 0.71; 95% CI 0.52 - 0.96). For the weekend-to-weekday sleep duration ratio (SDR), after univariate analysis, individuals were statistically significant 0.54 times less likely, and 1.5 times more likely to experience MI in those whose SDR is more than 1, and those whose SDR equals 1, respectively (95% CI SDR &gt; 1: 1.14, 1.98; SDR = 1: 0.39, 0.72). After adjusting, participants with SDR more than 1 were statistically significant 0.69 times less likely to develop MI. Conclusions Moderate sleep durations on weekdays (in Q3), weekends (in Q2), along with SDR more than 1, were negatively linked with MI in a general population. This implies that sleep durations on both weekends and weekdays have comparable associations with MI. Additionally, full recovery sleep on weekends following sleep-deprived weekdays, might reduce MI risk. Further studies are needed to explore impact of weekend and weekday sleep patterns on MI.Histogram and Margins plotTable of Odd ratios

Background: There is limited evidence regarding the impact of cardiac arrhythmias in patients with pulmonary arterial hypertension (PAH). We aim to comprehensively investigate the epidemiology and clinical outcomes of cardiac arrhythmias in patients with PAH. Methods: In a retrospective cohort study including 512 PAH patients from 2001-2021 at 3 Mayo Clinic sites, PAH patients were identified via echocardiogram, pulmonary function tests, and right heart catheterization. Demographic data at PAH diagnosis and clinical outcomes over a 10-year period were collected. The PAH patients were categorized into three groups based on arrhythmic onset: 1) patients with arrhythmia prior to PAH diagnosis, 2) patients diagnosed with arrhythmia during 10-year PAH follow-up, and 3) patients without arrhythmia during 10-year PAH follow-up. Survival outcomes were analyzed using multivariable Cox proportional hazards regression, adjusted with the REVEAL 2.0 score. Results: Among 512 PAH patients (mean age 56.1 years, 81.8% female), the prevalence of cardiac arrhythmias at PAH diagnosis was 10.5%. The cumulative incidences of new-onset arrhythmias at 1, 5, and 10 years were 6.6%, 18.4%, and 29.2%, respectively. Patients with arrhythmia diagnosed before and after PAH diagnosis showed significantly higher all-cause mortality rates with adjusted HR of 2.06 [95% CI 1.36-3.12] and 1.57 [95% CI 1.17-2.20] respectively (Figure 1). Similarly in both arrhythmic groups, there was a shorter median time to the first all-cause hospitalization (9.5 and 15.9 months vs. 21.2 months) and a higher number of all-cause hospitalizations (0.38 and 0.64 times per year vs. 0.10 times per year) compared to the non-arrhythmic group. Conclusions: Cardiac arrhythmias can develop in nearly one-third of PAH patients within 10 years of PAH diagnosis and independently contribute to increased mortality and hospitalization frequency.

Abstract Funding Acknowledgements Type of funding sources: None. Background/Introduction Idiopathic ventricular fibrillation (IVF) is responsible for 5-7% of sudden cardiac arrests in the absence of substrate for ventricular arrhythmia, structural diseases, or primary arrhythmic syndromes. The characteristics, management, and prognosis of these patients are unclear. Purpose To investigate the clinical features, management, and prognosis of IVF in our hospital healthcare system Methods Mayo Database Explorer software was used to identify IVF patients from our hospital electronic medical records between 1990 to 2022 in 5 states. The medical records were manually reviewed. Results A total of 132 patients were initially diagnosed with IVF. During the 9.2±6.8 years mean follow-up, 36 [27.3%] patients were later diagnosed with structural diseases or primary arrhythmic syndromes (dilated cardiomyopathy [41.7%], Long QT syndrome [27.8%], catecholaminergic polymorphic ventricular tachycardia [8.3%], Brugada syndrome [5.6%], mitral valve-related arrhythmia [5.6%], and short QT syndrome [2.8%]). Among the rest of the 96 patients with true IVF (mean age 38.4±15.7 years, male 59.4%, Caucasian 80.2%, hypertension 28.1%, diabetes 8.3%), 91 (94.8%) patients presented with out-of-hospital cardiac arrest and 88 (91.7%) patients had a history of syncope. Early repolarization and fragmented QRS were noted in 32 (33.3%) and 28 (29.1%) patients, respectively. Defibrillators were implanted in 92 (95.8%) patients. Genetic testing was performed in 35 (36.5%) patients, and possible associated mutations were found in 13 (37.1%) patients. An Electrophysiology study was conducted in 55 (57.3%) patients, and ventricular fibrillation was induced in 17 (30.9%) patients. The medical management with antiarrhythmic drugs was selected in 60 (62.5%) patients, and the catheter ablation ± anti-arrhythmic drugs was selected in 36 (37.5%) patients. The recurrence of ventricular fibrillation during 9.2±6.8 years of mean follow-up was significantly higher in the ablation strategy group (p=0.0003) (Figure 1). Conclusions We reported the largest cohort of IVF patients from a single healthcare system. Early repolarization and fragmented QRS were common in IVF. The possible associated mutations were found in one-third of IVF who underwent genetic testing. The ventricular fibrillation recurrences were significantly higher in the catheter ablation strategy group.

AbstractIntroductionBrugada syndrome is an inherited arrhythmic disease associated with major arrhythmic events (MAE). The importance of primary prevention of sudden cardiac death (SCD) in Brugada syndrome is well recognized; however, ventricular arrhythmia risk stratification remains challenging and controversial. We aimed to assess the association of type of syncope with MAE via systematic review and meta‐analysis.MethodsWe comprehensively searched the databases of MEDLINE and EMBASE from inception to December 2021. Included studies were cohort (prospective or retrospective) studies that reported the types of syncope (cardiac, unexplained, vasovagal, and undifferentiated) and MAE. Data from each study were combined using the random‐effects, generic inverse variance method of DerSimonian and Laird to calculate the odds ratio (OR) and 95% confidence intervals (CIs).ResultsSeventeen studies from 2005 to 2019 were included in this meta‐analysis involving 4355 Brugada syndrome patients. Overall, syncope was significantly associated with an increased risk of MAE in Brugada syndrome (OR = 3.90, 95% CI: 2.22–6.85, p < .001, I2 = 76.0%). By syncope type, cardiac (OR = 4.48, 95% CI: 2.87–7.01, p < .001, I2 = 0.0%) and unexplained (OR = 4.71, 95% CI: 1.34–16.57, p = .016, I2 = 37.3%) syncope was significantly associated with increased risk of MAE in Brugada syndrome. Vasovagal (OR = 2.90, 95% CI: 0.09–98.45, p = .554, I2 = 70.9%) and undifferentiated syncope (OR = 2.01, 95% CI: 1.00–4.03, p = .050, I2 = 64.6%, respectively) were not.ConclusionOur study demonstrated that cardiac and unexplained syncope was associated with MAE risk in Brugada syndrome populations but not in vasovagal syncope and undifferentiated syncope. Unexplained syncope is associated with a similar increased risk of MAE compared to cardiac syncope.