Delirium After Transcatheter Aortic Valve Replacement.

BACKGROUND: Postoperative delirium is associated with increased mortality. Patients undergoing transcatheter aortic valve replacement are at risk for delirium because of comorbid conditions. OBJECTIVE: To compare the incidence, odds, and mortality implications of delirium between patients undergoing transcatheter replacement and patients undergoing surgical replacement. METHODS: The Richmond Agitation-Sedation Scale and the Confusion Assessment Method for the Intensive Care Unit were used to assess arousal level and delirium prospectively in all patients with severe aortic stenosis who had transcatheter or surgical aortic valve replacement at an academic medical center. Multivariable logistic regression was used to determine the relationship between procedure type and occurrence of delirium. Cox regression was used to assess the association between postoperative delirium and 6-month mortality. RESULTS: A total of 105 patients had transcatheter replacement and 121 had surgical replacement. Patients in the transcatheter group were older (median age, 81 vs 68 years; P < .001) and had more comorbid conditions (median Charlson Comorbidity Index, 3 vs 2; P < .001). Patients in the transcatheter group also had lower incidence (19% vs 21%; P = .65) and odds of delirium developing (odds ratio, 0.4; 95% CI, 0.2-0.9; P = .03). Delirium was independently associated with a 3-fold higher mortality by 6 months (hazard ratio, 3.4; 95% CI, 1.3-8.8; P = .01). CONCLUSIONS: Delirium occurs in at least 1 in 5 patients after transcatheter or surgical aortic valve replacement. Delirium is less likely to develop in the transcatheter group but is associated with higher mortality in both groups.

Higher achieved mean arterial pressure during therapeutic hypothermia is not associated with neurologically intact survival following cardiac arrest.

INTRODUCTION: To determine if higher achieved mean arterial blood pressure (MAP) during treatment with therapeutic hypothermia (TH) is associated with neurologically intact survival following cardiac arrest. METHODS: Retrospective analysis of a prospectively collected cohort of 188 consecutive patients treated with TH in the cardiovascular intensive care unit of an academic tertiary care hospital. RESULTS: Neurologically intact survival was observed in 73/188 (38.8%) patients at hospital discharge and in 48/162 (29.6%) patients at a median follow up interval of 3 months. Patients in shock at the time of admission had lower baseline MAP at the initiation of TH (81 versus 87mmHg; p=0.002), but had similar achieved MAP during TH (80.3 versus 83.7mmHg; p=0.11). Shock on admission was associated with poor survival (18% versus 52%; p<0.001). Vasopressor use among all patients was common (84.6%) and was not associated with increased mortality. A multivariable analysis including age, initial rhythm, time to return of spontaneous circulation, baseline MAP and achieved MAP did not demonstrate a relationship between MAP achieved during TH and poor neurological outcome at hospital discharge (OR 1.28, 95% CI 0.40-4.06; p=0.87) or at outpatient follow up (OR 1.09, 95% CI 0.32-3.75; p=0.976). CONCLUSION: We did not observe a relationship between higher achieved MAP during TH and neurologically intact survival. However, shock at the time of admission was clearly associated with poor outcomes in our study population. These data do not support the use of vasopressors to artificially increase MAP in the absence of shock. There is a need for prospective, randomized trials to further define the optimum blood pressure target during treatment with TH.

Cardiovascular biomarkers and their utility in the older adult.

Cardiovascular disease is the leading cause of morbidity and mortality in individuals over the age of 65 yet diagnosis, risk stratification and management continue to be more challenging than in younger adults due to the vast heterogeneity seen in this population. The current literature validates the use of biomarkers in addition to traditional risk assessment tools in younger and middle aged adults. The evidence for biomarkers in this older population is sparse; this review examines the epidemiological association of current biomarkers in the field and the utility of these markers in the diagnosis, risk discrimination and management of cardiovascular disease.

Relation between infarct size in ST-segment elevation myocardial infarction treated successfully by percutaneous coronary intervention and left ventricular ejection fraction three months after the infarct.

The goal of this analysis was to determine the relation between myocardial infarct size and left ventricular (LV) ejection fraction (EF) in patients with ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (pPCI) using cardiovascular magnetic resonance imaging (CMR). After STEMI, LVEF and infarct size correlate with prognosis, but the relation between infarct size and LVEF is incompletely known. Consecutive subjects presenting to a single center with STEMI treated with pPCI were enrolled, and cine functional and late gadolinium enhancement CMR was performed 3 months after presentation. From cine images, LVEF was calculated using volumetric summation of disks method. Infarct size was measured as percent LV myocardial volume with late gadolinium enhancement. In the 78 patients enrolled (mean age 54.5 years, range 42 to 82), median LVEF was 56% (interquartile range 49 to 62) and median infarct size was 11% (interquartile range 5 to 18). Of the 53 patients with infarct size <15%, all had LVEF >40%, and there was no significant relation between infarct size and LVEF (slope -0.43, R(2) = 0.045, p = 0.13). In patients with infarct size > or =15%, there was a significant negative linear association between infarct size and LVEF (slope -1.21, R(2) = 0.66, p <0.001), such that for every 5% increase in infarct size, there was a 6.1% decrease in LVEF. In conclusion, there is a negative linear relation between infarct size and LVEF for moderate to large infarcts. For small infarcts there is no significant relation between infarct size and LVEF. Up to 15% of LV myocardial volume may be infarcted before there is any appreciable decrease in LVEF.