Timing and Outcomes After Coronary Angiography Following Out-of-Hospital Cardiac Arrest Without Signs of ST-Segment Elevation Myocardial Infarction.

BACKGROUND: There is broad consensus that resuscitated out-of-hospital cardiac arrest (OHCA) patients with ST-segment elevation myocardial infarction (STEMI) should receive immediate coronary angiography (CAG); however, factors that guide patient selection and optimal timing of CAG for post-arrest patients without evidence of STEMI remain incompletely described. OBJECTIVE: We sought to describe the timing of post-arrest CAG in actual practice, patient characteristics associated with decision to perform immediate vs. delayed CAG, and patient outcomes after CAG. METHODS: We conducted a retrospective cohort study at seven U.S. academic hospitals. Resuscitated adult patients with OHCA were included if they presented between January 1, 2015 and December 31, 2019 and received CAG during hospitalization. Emergency medical services run sheets and hospital records were analyzed. Patients without evidence of STEMI were grouped and compared based on time from arrival to CAG performance into "early" (≤ 6 h) and "delayed" (> 6 h). RESULTS: Two hundred twenty-one patients were included. Median time to CAG was 18.6 h (interquartile range [IQR] 1.5-94.6 h). Early catheterization was performed on 94 patients (42.5%) and delayed catheterization was performed on 127 patients (57.5%). Patients in the early group were older (61 years [IQR 55-70 years] vs. 57 years [IQR 47-65] years) and more likely to be male (79.8% vs. 59.8%). Those in the early group were more likely to have clinically significant lesions (58.5% vs. 39.4%) and receive revascularization (41.5% vs. 19.7%). Patients were more likely to die in the early group (47.9% vs. 33.1%). Among survivors, there was no significant difference in neurologic recovery at discharge. CONCLUSIONS: OHCA patients without evidence of STEMI who received early CAG were older and more likely to be male. This group was more likely to have intervenable lesions and receive revascularization.

CPAP, weight loss, or both for obstructive sleep apnea.

BACKGROUND: Obesity and obstructive sleep apnea tend to coexist and are associated with inflammation, insulin resistance, dyslipidemia, and high blood pressure, but their causal relation to these abnormalities is unclear. METHODS: We randomly assigned 181 patients with obesity, moderate-to-severe obstructive sleep apnea, and serum levels of C-reactive protein (CRP) greater than 1.0 mg per liter to receive treatment with continuous positive airway pressure (CPAP), a weight-loss intervention, or CPAP plus a weight-loss intervention for 24 weeks. We assessed the incremental effect of the combined interventions over each one alone on the CRP level (the primary end point), insulin sensitivity, lipid levels, and blood pressure. RESULTS: Among the 146 participants for whom there were follow-up data, those assigned to weight loss only and those assigned to the combined interventions had reductions in CRP levels, insulin resistance, and serum triglyceride levels. None of these changes were observed in the group receiving CPAP alone. Blood pressure was reduced in all three groups. No significant incremental effect on CRP levels was found for the combined interventions as compared with either weight loss or CPAP alone. Reductions in insulin resistance and serum triglyceride levels were greater in the combined-intervention group than in the group receiving CPAP only, but there were no significant differences in these values between the combined-intervention group and the weight-loss group. In per-protocol analyses, which included 90 participants who met prespecified criteria for adherence, the combined interventions resulted in a larger reduction in systolic blood pressure and mean arterial pressure than did either CPAP or weight loss alone. CONCLUSIONS: In adults with obesity and obstructive sleep apnea, CPAP combined with a weight-loss intervention did not reduce CRP levels more than either intervention alone. In secondary analyses, weight loss provided an incremental reduction in insulin resistance and serum triglyceride levels when combined with CPAP. In addition, adherence to a regimen of weight loss and CPAP may result in incremental reductions in blood pressure as compared with either intervention alone. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT0371293 .).

Depressive symptoms in patients with obstructive sleep apnea: biological mechanistic pathways.

This study examined the association between depressive symptoms, as well as depressive symptom dimensions, and three candidate biological pathways linking them to Obstructive sleep apnea (OSA): (1) inflammation; (2) circulating leptin; and (3) intermittent hypoxemia. Participants included 181 obese adults with moderate-to-severe OSA enrolled in the Cardiovascular Consequences of Sleep Apnea (COSA) trial. Depressive symptoms were measured using the Beck Depression Inventory-II (BDI-II). We assessed inflammation using C-reactive protein levels (CRP), circulating leptin by radioimmunoassay using a double antibody/PEG assay, and intermittent hypoxemia by the percentage of sleep time each patient had below 90% oxyhemoglobin saturation. We found no significant associations between BDI-II total or cognitive scores and CRP, leptin, or percentage of sleep time below 90% oxyhemoglobin saturation after controlling for relevant confounding factors. Somatic symptoms, however, were positively associated with percentage of sleep time below 90% saturation (ß = 0.202, P = 0.032), but not with CRP or circulating leptin in adjusted models. Another significant predictor of depressive symptoms included sleep efficiency (ßBDI Total = -0.230, P = 0.003; ßcognitive = -0.173, P = 0.030 (ßsomatic = -0.255, P = 0.001). In patients with moderate-to-severe OSA, intermittent hypoxia may play a role in somatic rather than cognitive or total depressive symptoms.

Clinical factors associated with significant coronary lesions following out-of-hospital cardiac arrest.

OBJECTIVES: Out-of-hospital cardiac arrest (OHCA) afflicts >350,000 people annually in the United States. While postarrest coronary angiography (CAG) with percutaneous coronary intervention (PCI) has been associated with improved survival in observational cohorts, substantial uncertainty exists regarding patient selection for postarrest CAG. We tested the hypothesis that symptoms consistent with acute coronary syndrome (ACS), including chest discomfort, prior to OHCAs are associated with significant coronary lesions identified on postarrest CAG. METHODS: We conducted a multicenter retrospective cohort study among eight regional hospitals. Adult patients who experienced atraumatic OHCA with successful initial resuscitation and subsequent CAG between January 2015 and December 2019 were included. We collected data on prehospital documentation of potential ACS symptoms prior to OHCA as well as clinical factors readily available during postarrest care. The primary outcome in multivariable regression modeling was the presence of significant coronary lesions (defined as >50% stenosis of left main or >75% stenosis of other coronary arteries). RESULTS: Four-hundred patients were included. Median (interquartile range) age was 59 (51-69) years; 31% were female. At least one significant stenosis was found in 62%, of whom 71% received PCI. Clinical factors independently associated with a significant lesion included a history of myocardial infarction (adjusted odds ratio [aOR] = 6.5, [95% confidence interval {CI} = 1.3 to 32.4], p = 0.02), prearrest chest discomfort (aOR = 4.8 [95% CI = 2.1 to 11.8], p ≤ 0.001), ST-segment elevations (aOR = 3.2 [95% CI = 1.7 to 6.3], p < 0.001), and an initial shockable rhythm (aOR = 1.9 [95% CI = 1.0 to 3.4], p = 0.05). CONCLUSIONS: Among survivors of OHCA receiving CAG, history of prearrest chest discomfort was significantly and independently associated with significant coronary artery lesions on postarrest CAG. This suggests that we may be able to use prearrest symptoms to better risk stratify patients following OHCA to decide who will benefit from invasive angiography.

Arterial pulsatile hemodynamic load induced by isometric exercise strongly predicts left ventricular mass in hypertension.

Although resting hemodynamic load has been extensively investigated as a determinant of left ventricular (LV) hypertrophy, little is known about the relationship between provoked hemodynamic load and the risk of LV hypertrophy. We studied central pressure-flow relations among 40 hypertensive and 19 normotensive adults using carotid applanation tonometry and Doppler echocardiography at rest and during a 40% maximal voluntary forearm contraction (handgrip) maneuver. Carotid-femoral pulse wave velocity (CF-PWV) was measured at rest. Hypertensive subjects demonstrated various abnormalities in resting and induced pulsatile load. Isometric exercise significantly increased systemic vascular resistance, aortic characteristic impedance (Zc), induced earlier wave reflections, increased augmentation index, and decreased total arterial compliance (TAC; all P < or = 0.01). In hypertensive subjects, CF-PWV was the strongest resting predictor of LV mass index (LVMI) and remained an independent predictor after adjustment for age, gender, systemic vascular resistance, reflection magnitude, aortic Zc, and TAC (beta = 2.52 m/s; P < 0.0001). Age, sex, CF-PWV, and resting hemodynamic indexes explained 48% of the interindividual variability in LVMI. In stepwise regression, TAC (beta = -17.85; P < 0.0001) during handgrip, Zc during handgrip (beta = -150; P < 0.0001), and the change in the timing of wave reflections during handgrip (beta = -0.63; P = 0.03) were independent predictors of LVMI. A model that included indexes of provoked hemodynamic load explained 68% of the interindividual variability in LVMI. Hemodynamic load provoked by isometric exercise strongly predicts LVMI in hypertension. The magnitude of this association is far greater than for resting hemodynamic load, suggesting that provoked testing captures important arterial properties that are not apparent at rest and is advantageous to assess dynamic arterial load in hypertension.

Effect of CPAP, Weight Loss, or CPAP Plus Weight Loss on Central Hemodynamics and Arterial Stiffness.

Obesity and obstructive sleep apnea tend to coexist. Little is known about the effects of obstructive sleep apnea, obesity, or their treatment on central aortic pressures and large artery stiffness. We randomized 139 adults with obesity (body mass index >30 kg/m2) and moderate-to-severe obstructive sleep apnea to (1) continuous positive airway pressure (CPAP) therapy (n=45), (2) weight loss (WL) therapy (n=48), or (3) combined CPAP and WL (n=46) for 24 weeks. We assessed the effect of these interventions on central pressures and carotid-femoral pulse wave velocity (a measure of large artery stiffness), measured with arterial tonometry. Central systolic pressure was reduced significantly only in the combination arm (-7.4 mm Hg; 95% confidence interval, -12.5 to -2.4 mm Hg; P=0.004), without significant reductions detected in either the WL-only (-2.3 mm Hg; 95% confidence interval, -7.5 to 3.0; P=0.39) or the CPAP-only (-3.1 mm Hg; 95% confidence interval, -8.3 to 2.0; P=0.23) arms. However, none of these interventions significantly changed central pulse pressure, pulse pressure amplification, or the central augmentation index. The change in mean arterial pressure (P=0.008) and heart rate (P=0.027) induced by the interventions was significant predictors of the change in carotid-femoral pulse wave velocity. However, after adjustment for mean arterial pressure and heart rate, no significant changes in carotid-femoral pulse wave velocity were observed in any group. In obese subjects with obstructive sleep apnea, combination therapy with WL and CPAP is effective in reducing central systolic pressure. However, this effect is largely mediated by changes in mean, rather than central pulse pressure. WL and CPAP, alone or in combination, did not reduce large artery stiffness in this population. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00371293.

Normative values and correlates of carotid artery intima-media thickness and carotid atherosclerosis in Andean-Hispanics: The Prevencion Study.

OBJECTIVES: Carotid intima-media thickness (cIMT) is an independent predictor of cardiovascular risk. Furthermore, ethnicity and gender-specific normative data are required to assess cIMT, which are not available for Andean-Hispanics. In addition, data regarding correlates of subclinical atherosclerosis in ethnic population are needed. METHODS: We studied 1448 adults enrolled in a population-based study in Peru. cIMT and carotid plaque were measured with high-resolution ultrasonography. A healthy reference sample (n=472) with no cardiovascular disease, normal weight and normal metabolic parameters was selected to establish normative cIMT values. Correlates of abnormal cIMT and carotid plaque were assessed in the entire population. RESULTS: In the reference sample, 95th-percentile cIMT values were both age and gender-dependent. In stepwise regression, selected predictors of increasing cIMT were: older age, impaired fasting glucose, diabetes mellitus, higher systolic blood pressure, higher LDL-cholesterol, smoking and male gender. Predictors of carotid plaque included older age, male gender, higher systolic blood pressure, lower diastolic blood pressure and higher LDL-cholesterol. HDL-cholesterol and C-reactive protein were not associated with cIMT or carotid plaque. The lack of association with HDL-cholesterol was confirmed using high performance liquid chromatography. CONCLUSIONS: We present ethnic-specific cut-offs for abnormal cIMT applicable to Andean-Hispanics and correlates of subclinical atherosclerosis in this population. Pending longitudinal studies, our data supports several risk associations seen in other populations and can be used to identify Andean-Hispanics at increased risk for atherosclerotic cardiovascular disease. The lack of association between HDL-C and cIMT or carotid plaque in this population requires further investigation.