Relationship Between Caffeine Consumption and Young Athletes' Comorbidities, Exercise-Related Symptoms, and Baseline Electrocardiogram.

BACKGROUND: Caffeine consumption causes diverse physiologic effects that can affect athletes both positively and negatively. There is a lack of research investigating the long-term effects of caffeine intake on exercise and on overall cardiovascular health in young athletes. HYPOTHESIS: Certain characteristics such as age, body mass index (BMI), race, and medical diagnoses are associated with increased caffeine use, and there is a relationship between caffeine consumption and symptoms during exercise and cardiovascular abnormalities in young athletes. STUDY DESIGN: Cross-sectional study. LEVEL OF EVIDENCE: Level 4. METHODS: This study utilized the HeartBytes National Youth Cardiac Registry to collect data related to demographics, caffeine use, and physical examination and electrocardiogram (ECG) findings of 7425 12- to 20-year-olds (60.6% male, 39.4% female) who attended a Simon's Heart cardiac screening event between 2014 and 2021. Univariable and multivariable logistic regression models were used for analysis. RESULTS: Persons who consumed caffeine were more likely to have attention deficit hyperactivity disorder (ADHD) (adjusted odds ratio [aOR], 1.43; CI, 1.15-1.76]; P < 0.01) and more likely to have a BMI ≥30 kg/m2 (aOR, 1.69; CI, 1.27-2.25]; P < 0.01) compared with nondrinkers. After controlling for age, gender, race, and BMI, there were no significant differences in symptoms during exercise (aOR, 1.27; CI, 0.97-1.66; P = 0.08) or abnormal ECG findings (OR, 0.93; CI, 0.66-1.31; P = 0.70) between those who consume caffeine and those who do not. CONCLUSION: Caffeine consumption was associated with increased BMI and increased likelihood of having ADHD; however, caffeine use overall was not associated with increased risk of symptoms during exercise or ECG abnormalities. CLINICAL RELEVANCE: Whereas caffeine consumption overall did not increase risk of exercise-related symptoms, soda drinkers were at higher risk for symptoms during exercise, and coffee drinkers were at higher risk of syncope with exercise. Prospective studies with longitudinal follow-up and more specific outcomes data is the next step in qualifying the impact of caffeine on young athletes.

PCI for acute myocardial infarction in patients with a pre-existing LVAD, does it improve survival?

BACKGROUND: It is well established that percutaneous coronary intervention (PCI) is a life-saving procedure for acute myocardial infarction (AMI) in the general population and is guideline-recommended for both STEMI and NSTEMI. There is little literature regarding its use in patients with a pre-implanted Left Ventricular Assist Device (LVAD). METHODS: We retrospectively analyzed data from the National Inpatient Sample (NIS) Database to select all US adult patients (>18 years) with an LVAD diagnosed with an AMI divided into two groups; those who received PCI during the hospitalization and those who did not. RESULTS: A total of 3722 LVAD patients with AMI were identified, of these 17% of patients received PCI and 83% did not. After propensity matching of LVAD patients with AMI, there were 626 patients who received PCI and 623 who did not. Of patients receiving PCI, 37.5% had a STEMI while 29.7% of patients who did not receive PCI had STEMI. Rates of kidney injury (36.5% vs. 43.3%, OR 0.75, 95% CI 0.60-0.94, p = 0.016), sepsis (3.2% vs. 11.4%, OR 0.26, 95% CI 0.15-0.43, p < 0.001), cardiogenic shock (44.1% vs. 50.4%, OR 0.78, 95% CI 0.62-0.97, p = 0.03) and mortality (17.4% vs. 28.9%, OR 0.52, 95% CI 0.40-0.68, p < 0.001) were all better for patients receiving PCI. Vascular complications (1.4% vs. 0%, p = 0.008) and intracerebral hemorrhage (ICH) (1.6% vs. 0, p = 0.004) were both more common in the group receiving PCI. CONCLUSIONS: In this study, patients supported by LVAD with AMI had an elevated risk of mortality compared to generally accepted mortality rates of patients without LVAD. In this analysis PCI was associated with a decreased risk of mortality, cardiogenic shock, and kidney injury while increasing the risk for vascular complications and intracranial hemorrhage.

Data supporting characterization of CLIC1, CLIC4, CLIC5 and DmCLIC antibodies and localization of CLICs in endoplasmic reticulum of cardiomyocytes.

Chloride intracellular channel (CLICs) proteins show 60-70% sequence identity to each other, and exclusively localize to the intracellular organelle membranes and cytosol. In support of our recent publication, "Molecular identity of cardiac mitochondrial chloride intracellular channel proteins" (Ponnalagu et al., 2016) [1], it was important to characterize the specificity of different CLIC paralogs/ortholog (CLIC1, CLIC4, CLIC5 and DmCLIC) antibodies used to decipher their localization in cardiac cells. In addition, localization of CLICs in the other organelles such as endoplasmic reticulum (ER) of cardiomyocytes was established. This article also provides data on the different primers used to show the relative abundance of CLIC paralogs in cardiac tissue and the specificity of the various CLIC antibodies used. We demonstrate that the predominant CLICs in the heart, namely CLIC1, CLIC4 and CLIC5, show differential distribution in endoplasmic reticulum. CLIC1 and CLIC4 both show co-localization to the endoplasmic reticulum whereas CLIC5 does not.

Molecular identity of cardiac mitochondrial chloride intracellular channel proteins.

Emerging evidences demonstrate significance of chloride channels in cardiac function and cardioprotection from ischemia-reperfusion (IR) injury. Unlike mitochondrial potassium channels sensitive to calcium (BKCa) and ATP (KATP), molecular identity of majority of cardiac mitochondrial chloride channels located at the inner membrane is not known. In this study, we report the presence of unique dimorphic chloride intracellular channel (CLIC) proteins namely CLIC1, CLIC4 and CLIC5 as abundant CLICs in the rodent heart. Further, CLIC4, CLIC5, and an ortholog present in Drosophila (DmCLIC) localize to adult cardiac mitochondria. We found that CLIC4 is enriched in the outer mitochondrial membrane, whereas CLIC5 is present in the inner mitochondrial membrane. Also, CLIC5 plays a direct role in regulating mitochondrial reactive oxygen species (ROS) generation. Our study highlights that CLIC5 is localized to the cardiac mitochondria and directly modulates mitochondrial function.