Venoarterial extracorporeal membrane oxygenation (VA ECMO) provides mechanical support to the patient with cardiac or cardiopulmonary failure. This paper reviews the physiology of VA ECMO including the determinants of ECMO flow and gas exchange. The efficacy of this therapy may be determined by assessing patient hemodynamics and device flow, overall gas exchange support, markers of adequate oxygen delivery, and pulsatility of the arterial blood pressure waveform.
In-hospital mortality for CS has declined but remains high. Rates of CS have outpaced MCS utilisation which remains uncommon in non-MI hospitalisations with shock. MCS is associated with utilisation of other procedures during hospitalisation.
The pandemic of heart failure and the limited options for treatment of end-stage disease have resulted in an increase in the utilization of left ventricular assist devices (LVADs). Improvements in device technology and patient survival have led to an expanding population of patients requiring noncardiac surgery while on LVAD therapy, thus leading to a growing need for familiarity with the physiology of these patients. This review describes the functional mechanics of the most prevalent continuous-flow LVAD, the HeartMate II, and focuses on perioperative anesthetic concerns.
Objectives: To characterize the impact of obesity on disease severity in patients with coronavirus disease 2019. Design: This was a retrospective cohort study designed to evaluate the association between body mass index and risk of severe disease in patients with coronavirus disease 2019. Data were abstracted from the electronic health record. The primary endpoint was a composite of intubation or death. Setting: Two hospitals in Massachusetts (one quaternary referral center and one affiliated community hospital). Patients: Consecutive patients hospitalized with confirmed coronavirus disease 2019 admitted between March 13, 2020, and April 3, 2020. Interventions: None. Measurements and Main Results: A total of 305 patients were included in this study. We stratified patients by body mass index category: < 25 kg/m 2 (54 patients, 18%), ≥ 25 kg/m 2 to < 30 kg/m 2 (124 patients, 41%), ≥ 30 kg/m 2 to < 35 kg/m 2 (58 patients, 19%), and ≥ 35 kg/m 2 (69 patients, 23%). In total, 128 patients (42%) had a primary endpoint (119 patients [39%] were intubated and nine died [3%] without intubation). Sixty-five patients (51%) with body mass index greater than or equal to 30 kg/m 2 were intubated or died. Adjusted Cox models demonstrated that body mass index greater than or equal to 30 kg/m 2 was associated with a 2.3-fold increased risk of intubation or death (95% CI, 1.2–4.3) compared with individuals with body mass index less than 25 kg/m 2 . Diabetes was also independently associated with risk of intubation or death (hazard ratio, 1.8; 95% CI, 1.2–2.7). Fifty-six out of 127 patients (44%) with body mass index greater than or equal to 30 kg/m 2 had diabetes, and the combination of both diabetes and body mass index greater than or equal to 30 kg/m 2 was associated with a 4.5-fold increased risk of intubation or death (95% CI, 2.0–10.2) compared with patients without diabetes and body mass index less than 25 kg/m 2 . Conclusions: Among consecutive patients hospitalized with coronavirus disease 2019, obesity was an independent risk factor for intubation or death.
and the loss of hypoxic pulmonary vasoconstriction play a pivotal role in the pathophysiology of coronavirus disease 2019 (COVID-19) respiratory distress. 1,2 Dihydropyridine calcium channel blockers (CCBs), frequently prescribed first-line antihypertensive agents, have the potential to disrupt hypoxic pulmonary vasoconstriction 3 and worsen V_/Q_ mismatch that leads to profound hypoxemia in patients with pulmonary disease. 4 We hypothesized that CCBs would be associated with worse respiratory failure in patients with COVID-19. MethodsAmong 444 consecutively hospitalized patients with confirmed COVID-19 (admitted between March 13 and April 7, 2020, at a quaternary referral center and an affiliated community hospital in Massachusetts), 245 patients had hypertension and were included in the analysis. Data elements were abstracted retrospectively from the electronic health record by trained study personnel who followed standardized protocol. The study was approved by the Partners Healthcare Institutional Review Board with a waiver of informed consent.Dihydropyridine CCB exposure status was based on confirmed home medication list at the time of hospital admission. The primary end point was a composite of intubation or death modeled as a time-to-event analysis. 5 For patients who died after intubation, the time of intubation was considered time of primary end point as with previous studies. 5 Cox models were used to evaluate the association between CCBs and the primary end point. Models were adjusted for age, sex, race/ethnicity, BMI, diabetes mellitus, coronary artery disease, heart failure, pulmonary hypertension, chronic kidney disease, asthma/COPD, peripheral arterial disease, Charlson Comorbidity Index, and the following medications: angiotensinconverting enzyme inhibitor/angiotensin receptor blocker, thiazide diuretic, loop diuretic, beta blocker, aspirin, and statin. To further account for potential confounding, an additional analysis was performed with propensity score matching. The propensity score for CCB use was estimated with a logistic regression model that incorporated the same covariates used in the multivariable Cox model.
Background-Carotid intima-media thickness (CIMT) is highly heritable and associated with stroke and myocardial infarction, making it a promising quantitative intermediate phenotype for genetic studies of vascular disease. There have been many CIMT candidate gene association studies, but no systematic review to identify consistent, reliable findings. Methods and Results-We comprehensively sought all published studies of association between CIMT and any genetic polymorphism. We obtained additional unpublished data and performed meta-analyses for the 5 most commonly studied genes (studied in at least 2 studies in a total of Ͼ5000 subjects). We used a 3-step meta-analysis method: meta-analysis of variance; genetic model selection; and random effects meta-analysis of the mean CIMT difference between genotypes. We performed subgroup analyses to investigate effects of ethnicity, vascular risk status, and study size. We accounted for potential reporting bias by assessing qualitatively the possible effects of including unavailable data. Polymorphisms in 3 of the 5 genes (apolipoprotein E, angiotensin I converting enzyme, and 5,10-methylenetetrahydrofolate reductase) had an apparent association with CIMT, but for all these, we found evidence of small study bias. Apolipoprotein E 2/3/4 was the only polymorphism with a persistent, statistically significant but modest association when we restricted analysis to larger studies (Ͼ1000 subjects). Conclusions-Of the most extensively studied polymorphisms, apolipoprotein E 2/3/4 is the only one so far with a convincing association with CIMT. Larger studies than have generally been performed so far may be needed to confirm the associations identified in future genome-wide association studies, and to investigate modification of effect according to characteristics such as ethnicity and vascular risk status. (Circ Cardiovasc Genet. 2010;3:15-21.)Key Words: carotid arteries Ⅲ genetics Ⅲ meta-analysis S tudying intermediate, quantitative traits is a potentially useful approach to identify genetic risk factors for ischemic stroke and ischemic heart disease. 1 Carotid intima-media thickness (CIMT) is an intermediate phenotype for early atherosclerosis, is a strong predictor of future vascular events, including myocardial infarction and ischemic stroke, and is significantly greater in large artery (atherothrombotic) than small artery ischemic stroke. [2][3][4] Estimates of its heritability range from 30% to 86%. [5][6][7] Clinical Perspective on p 21There have been many studies on the effects of a range of candidate genes on CIMT, the results of which could provide useful insights into genetic influences on atherothrombotic disease and on large artery ischemic stroke and ischemic heart disease. We aimed to identify all published studies of the influence of any genetic polymorphism on CIMT and, for the most commonly studied polymorphisms, to carry out detailed methodological appraisals and meta-analyses of relevant studies. In doing so, we aimed to establish which candidate gene polymorphis...
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