Prospective Bidirectional Relationship Between Sleep Duration and Posttraumatic Stress Disorder Symptoms After Suspected Acute Coronary Syndrome.

OBJECTIVE: Sleep disturbance is a "hallmark" symptom of posttraumatic stress disorder (PTSD). Poor sleep (including short sleep) after combat-related trauma can also predict subsequent PTSD. Less is known about the association between sleep duration and PTSD symptoms when PTSD is induced by acute coronary syndrome (ACS). We examined the bidirectional relationship between sleep duration and PTSD symptoms over the year after hospital evaluation for ACS. METHODS: Participants were enrolled in this observational study after emergency department evaluation for ACS. Sleep duration ("During the past month, how many hours of actual sleep did you get at night?") and cardiac event or hospitalization-induced PTSD symptoms (PTSD Checklist) were assessed at 1, 6, and 12 months after hospital discharge. Cross-lagged path analysis was used to model the effects of sleep duration and PTSD symptoms on each other. Covariates included age, sex, race/ethnicity, cardiac severity, baseline depression symptoms, and early acute stress disorder symptoms. RESULTS: The sample included 1145 participants; 16% screened positive for probable PTSD (PTSD Checklist score ≥33). Mean sleep duration across time points was 6.1 hours. Higher PTSD symptoms predicted shorter sleep duration at the next time point (i.e., 1-6 and 6-12 months; B = -0.14 hours/10-point difference, SE = 0.03, p < .001). Shorter sleep duration was associated with higher PTSD symptoms at the next time point (B = -0.25 points/hour, SE = 0.12, p = .04). CONCLUSIONS: Short sleep duration and PTSD symptoms are mutually reinforcing across the first year after ACS evaluation. Findings suggest that sleep, PTSD symptoms, and their relationship should be considered in the post-ACS period.

Racial and Ethnic Differences in Presentation and Outcomes for Patients Hospitalized With COVID-19: Findings From the American Heart Association's COVID-19 Cardiovascular Disease Registry.

BACKGROUND: The coronavirus disease 2019 (COVID-19) pandemic has exposed longstanding racial and ethnic inequities in health risks and outcomes in the United States. We aimed to identify racial and ethnic differences in presentation and outcomes for patients hospitalized with COVID-19. METHODS: The American Heart Association COVID-19 Cardiovascular Disease Registry is a retrospective observational registry capturing consecutive patients hospitalized with COVID-19. We present data on the first 7868 patients by race/ethnicity treated at 88 hospitals across the United States between January 17, 2020, and July 22, 2020. The primary outcome was in-hospital mortality. Secondary outcomes included major adverse cardiovascular events (death, myocardial infarction, stroke, heart failure) and COVID-19 cardiorespiratory ordinal severity score (worst to best: death, cardiac arrest, mechanical ventilation with mechanical circulatory support, mechanical ventilation with vasopressors/inotrope support, mechanical ventilation without hemodynamic support, and hospitalization alone. Multivariable logistic regression analyses were performed to assess the relationship between race/ethnicity and each outcome adjusting for differences in sociodemographic, clinical, and presentation features, and accounting for clustering by hospital. RESULTS: Among 7868 patients hospitalized with COVID-19, 33.0% were Hispanic, 25.5% were non-Hispanic Black, 6.3% were Asian, and 35.2% were non-Hispanic White. Hispanic and Black patients were younger than non-Hispanic White and Asian patients and were more likely to be uninsured. Black patients had the highest prevalence of obesity, hypertension, and diabetes. Black patients also had the highest rates of mechanical ventilation (23.2%) and renal replacement therapy (6.6%) but the lowest rates of remdesivir use (6.1%). Overall mortality was 18.4% with 53% of all deaths occurring in Black and Hispanic patients. The adjusted odds ratios for mortality were 0.93 (95% CI, 0.76-1.14) for Black patients, 0.90 (95% CI, 0.73-1.11) for Hispanic patients, and 1.31 (95% CI, 0.96-1.80) for Asian patients compared with non-Hispanic White patients. The median odds ratio across hospitals was 1.99 (95% CI, 1.74-2.48). Results were similar for major adverse cardiovascular events. Asian patients had the highest COVID-19 cardiorespiratory severity at presentation (adjusted odds ratio, 1.48 [95% CI, 1.16-1.90]). CONCLUSIONS: Although in-hospital mortality and major adverse cardiovascular events did not differ by race/ethnicity after adjustment, Black and Hispanic patients bore a greater burden of mortality and morbidity because of their disproportionate representation among COVID-19 hospitalizations.

Association of Serum Aldosterone and Plasma Renin Activity With Ambulatory Blood Pressure in African Americans: The Jackson Heart Study.

BACKGROUND: The renin-angiotensin-aldosterone system (RAAS) is an important driver of blood pressure (BP), but the association of the RAAS with ambulatory BP (ABP) and ABP monitoring phenotypes among African Americans has not been assessed. METHODS: ABP and ABP monitoring phenotypes were assessed in 912 Jackson Heart Study participants with aldosterone and plasma renin activity (PRA). Multivariable linear and logistic regression analyses were used to analyze the association of aldosterone and PRA with clinic, awake, and asleep systolic BP and diastolic BP (DBP) and ABP monitoring phenotypes, adjusting for important confounders. RESULTS: The mean age of participants was 59±11 years and 69% were female. In fully adjusted models, lower log-PRA was associated with higher clinic, awake, and asleep systolic BP and DBP (all P<0.05). A higher log-aldosterone was associated with higher clinic, awake, and asleep DBP (all P<0.05). A 1-unit higher log-PRA was associated with lower odds of daytime hypertension (odds ratio [OR] 0.59 [95% CI, 0.49-0.71]), nocturnal hypertension (OR, 0.68 [95% CI, 0.58-0.79]), daytime and nocturnal hypertension (OR, 0.59 [95% CI, 0.48-0.71]), sustained hypertension (OR, 0.52 [95% CI, 0.39-0.70]), and masked hypertension (OR 0.75 [95% CI, 0.62-0.90]). A 1-unit higher log-aldosterone was associated with higher odds of nocturnal hypertension (OR, 1.38 [95% CI, 1.05-1.81]). Neither PRA nor aldosterone was associated with percent dipping, nondipping BP pattern, or white-coat hypertension. Patterns for aldosterone:renin ratio were similar to patterns for PRA. CONCLUSIONS: Suppressed renin activity and higher aldosterone:renin ratios were associated with higher systolic BP and DBP in the office and during the awake and asleep periods as evidenced by ABP monitoring. Higher aldosterone levels were associated with higher DBP, but not systolic BP, in the clinic and during the awake and asleep periods. Further clinical investigation of novel and approved medications that target low renin physiology such as epithelial sodium channel inhibitors and mineralocorticoid receptor antagonists may be paramount in improving hypertension control in African Americans.

Association of plasma endothelin-1 with blood pressure progression among Blacks: The Jackson Heart Study.

BACKGROUND: Despite pathophysiological links between endothelin (ET)-1 and hypertension in Black adults, there is no population-based data appraising the association of plasma ET-1 with longitudinal blood pressure (BP) changes in Blacks. METHODS: We analyzed data from 1197 Jackson Heart Study participants without hypertension (mean age 47.8 years [SD: 12.0]; 64.2% women), with plasma ET-1 available at the baseline examination (2000-2004). Poisson regression with robust variance was used to generate risk ratios (RRs) and 95% confidence intervals (CIs) of BP progression (an increase by ≥1 BP category based on the 2017 American College of Cardiology/American Heart Association classification) and incident hypertension (BP ≥ 130/80 mm Hg or use of antihypertensive medication) at follow-up (2005-2008 or 2009-2013). RESULTS: Over a median follow-up of 7 years (range: 4-11), 71.2% (n = 854) progressed to a higher BP stage and 64.6% (n = 773) developed hypertension. After adjusting for possible confounders, each unit increment in baseline log (ET-1) was associated with higher risks of BP progression (RR 1.15 [95% CI 1.03-1.29], P = .016) and incident hypertension (RR 1.15 [95% CI 1.01-1.31], P = .032). Compared to those in the lowest ET-1 quartile, participants in the highest quartile had significantly higher risks of BP progression (RR 1.20 [95% CI 1.05-1.37], P = .007) and incident hypertension (RR 1.16 [95% CI 1.00-1.36], P = .052). CONCLUSIONS: In a large, community-based sample of African Americans, higher plasma ET-1 concentrations were associated with higher risks of BP progression and incident hypertension.

Association Between Sleep Apnea and Blood Pressure Control Among Blacks.

BACKGROUND: Blacks have a high prevalence of hypertension and uncontrolled blood pressure (BP), each of which may be partially explained by untreated sleep apnea. We investigated the association of sleep apnea with uncontrolled BP and resistant hypertension in blacks. METHODS: Between 2012 and 2016, Jackson Heart Sleep Study participants (N=913) underwent an in-home Type 3 sleep apnea study, clinic BP measurements, and anthropometry. Moderate or severe obstructive sleep apnea (OSA) was defined as a respiratory event index ≥15, and nocturnal hypoxemia was quantified as percent sleep time with <90% oxyhemoglobin saturation. Prevalent hypertension was defined as either a systolic BP ≥130 mm Hg or diastolic BP >80mm Hg, use of antihypertensive medication, or self-report of a diagnosis of hypertension. Controlled BP was defined as systolic BP <130 mm Hg and diastolic BP <80 mm Hg; uncontrolled BP as systolic BP ≥130 mm Hg or diastolic BP ≥80 mm Hg with use of 1 to 2 classes of antihypertensive medication; and resistant BP as systolic BP ≥130 mm Hg or diastolic BP ≥80 mm Hg with the use of ≥3 classes of antihypertensive medication (including a diuretic) or use of ≥4 classes of antihypertensive medication regardless of BP level. Multinomial logistic regression models were fit to determine the association between OSA severity and uncontrolled BP or resistant hypertension (versus controlled BP) after multivariable adjustment. RESULTS: The analytic sample with hypertension (N=664) had a mean age of 64.0 (SD,10.6) years, and were predominately female (69.1%), obese (58.6%), and college educated (51.3%). Among the sample, 25.7% had OSA, which was untreated in 94% of participants. Overall, 48% of participants had uncontrolled hypertension and 14% had resistant hypertension. After adjustment for confounders, participants with moderate or severe OSA had a 2.0 times higher odds of resistant hypertension (95% confidence interval [CI], 1.14-3.67). Each standard deviation higher than <90% oxyhemoglobin saturation was associated with an adjusted odds ratio for resistant hypertension of 1.25 (95% CI 1.01-1.55). OSA and <90% oxyhemoglobin saturation were not associated with uncontrolled BP. CONCLUSION: Untreated moderate or severe OSA is associated with increased odds of resistant hypertension. These results suggest that untreated OSA may contribute to inadequate BP control in blacks.

The cardiac intensive care unit and the cardiac intensivist during the COVID-19 surge in New York City.

Critical care cardiology has been impacted by the coronavirus disease-2019 (COVID-19) pandemic. COVID-19 causes severe acute respiratory distress syndrome, acute kidney injury, as well as several cardiovascular complications including myocarditis, venous thromboembolic disease, cardiogenic shock, and cardiac arrest. The cardiac intensive care unit is rapidly evolving as the need for critical care beds increases. Herein, we describe the changes to the cardiac intensive care unit and the evolving role of critical care cardiologists and other clinicians in the care of these complex patients affected by the COVID-19 pandemic. These include practical recommendations regarding structural and organizational changes to facilitate care of patients with COVID-19; staffing and personnel changes; and health and safety of personnel. We draw upon our own experiences at NewYork-Presbyterian Columbia University Irving Medical Center to offer insights into the unique challenges facing critical care clinicians and provide recommendations of how to address these challenges during this unprecedented time.

Short Sleep Duration After Hospital Evaluation for Acute Coronary Syndrome Is Associated With Increased Risk of 6-Month Readmission.

OBJECTIVE: Hospital readmission after acute coronary syndrome (ACS) is associated with worsened patient outcomes and financial burden. Short sleep duration is a risk factor for cardiovascular events and may therefore represent a behavioral factor that increases risk of adverse posthospitalization outcomes. This study examined whether short sleep duration in the month after hospital evaluation for ACS is associated with 6-month all-cause emergency department (ED) and hospital readmission. METHODS: The current analyses entail a secondary analysis of a larger prospective observational cohort study. Sleep duration during the month after hospital evaluation for ACS was assessed subjectively and dichotomized as short (<6 hours) or not short (≥6 hours). A Cox proportional hazards model was used to assess the association between short sleep duration during the month after ACS hospital evaluation and 6-month all-cause ED/hospital readmission. RESULTS: A total of 576 participants with complete data were included in analyses. Approximately 34% of participants reported short sleep duration during the month after ACS evaluation. Short sleep duration was significantly associated with 6-month all-cause ED/hospital readmission (hazard ratio = 2.03; 95% confidence interval = 1.12-3.66) in the model adjusted for age, sex, race/ethnicity, clinical severity, cardiac and renal markers, depression, acute stress, and including a sleep duration by ACS status interaction. CONCLUSIONS: Short sleep duration after ACS hospital evaluation is prevalent and is associated with increased risk of all-cause readmission within 6 months of discharge. Current findings suggest that short sleep duration is an important modifiable behavioral factor to consider after hospital evaluation for ACS.

Occupational standing and change in the Ankle-Brachial Index: the Jackson Heart Study.

BACKGROUND: A growing interest in reducing occupational sitting has resulted in public health efforts to encourage intermittent standing in workplaces. However, concerns have been raised that standing for prolonged periods may expose individuals to new health hazards, including lower limb atherosclerosis. These concerns have yet to be corroborated or refuted. The purpose of this study was to investigate the association between occupational standing and adverse changes in the Ankle-Brachial Index (ABI). METHODS: We studied 2121 participants from the Jackson Heart Study, a single-site community-based study of African-Americans residing in Jackson, MS. Occupational standing ('never/seldom', 'sometimes', 'often/always') was self-reported at baseline (2000-2004). ABI was measured at baseline and again at follow-up (2009-2013). RESULTS: Over a median follow-up of 8 years, 247 participants (11.6%) exhibited a significant decline in ABI (eg, ABI decline >0.15). In multivariable-adjusted models, higher occupational standing was not significantly associated with ABI decline (occupational standing sometimes vs never/seldom: OR 1.05; 95% CI 0.67, 1.66; occupational standing often/always vs never/seldom: OR 1.22; 95% CI 0.77, 1.94). Similarly, higher occupational standing was not associated with low ABI at follow-up reflective of peripheral artery disease (ABI <0.90) or high ABI at follow-up reflective of incompressible vessels (ABI >1.40). CONCLUSIONS: In this community-based study of African-Americans, we found no evidence that occupational standing is deleteriously associated with adverse changes in ABI over a median follow-up of 8.0 years. These findings do not provide evidence implicating occupational standing as a risk factor for lower limb atherosclerosis.

Masked Hypertension: Whom and How to Screen?

PURPOSE OF REVIEW: To review issues regarding the practical implementation of screening strategies for masked hypertension. RECENT FINDINGS: Masked hypertension has been associated with an increased risk of cardiovascular disease events and all-cause mortality. Recent guidelines have encouraged practitioners to use out-of-clinic monitoring to detect masked hypertension in some situations. However, it is unclear from these guidelines who should be screened or how to best measure out-of-office blood pressure. In this review, challenges to screening strategies for masked hypertension, and factors that should be considered when deciding to screen using ambulatory or home blood pressure monitoring. Masked hypertension is an important clinical phenotype to detect. Future research is needed in order to develop optimal screening strategies, and to understand population level implications of using ambulatory or home blood pressure monitoring on blood pressure control.

Sleep Duration and Blood Pressure: Recent Advances and Future Directions.

PURPOSE OF REVIEW: This review discusses the recent literature on subjectively and objectively assessed sleep duration in relation to hypertension risk and out-of-clinic blood pressure (BP) measures and highlights critical areas for future research. RECENT FINDINGS: Sleep duration, particularly short sleep, may influence BP through disturbed autonomic balance, hormonal imbalances, increased adiposity and metabolic dysfunction, and disrupted circadian rhythms. Observational studies indicate that short and long sleep are associated with hypertension risk, reduced nocturnal dipping, and elevated morning BP, but evidence is stronger for short sleep. Experimental sleep restriction increases BP, while sleep extension may lower BP in prehypertensive individuals. Women and racial/ethnic minorities are more prone to the detrimental effects of short sleep on BP. Additional studies are warranted to clarify the association of objectively assessed sleep with BP level and diurnal pattern and to determine the sex- and race-specific effects of sleep restriction and extension on BP.