Purpose: the relationship between arterial carbon dioxide (CO2), cerebral saturation (SctO2) and patient survival has been poorly investigated in post-cardiac arrest patients. Current guidelines recommend to target CO2 levels between 40-45 mmHg although some authors recommend higher CO2 levels based on the hypothesis that hypercapnia may lead to increased cerebral perfusion. Therefore the aims of the present study were to explore the relationships between CO2, SctO2 and survival. Methods: Prospective observational study in 82 post-cardiac arrest patients treated with therapeutic hypothermia. Blood gasses were obtained with a 1 hour interval during the first 24 hours after admission. Cerebral saturation was monitored every 2 seconds with near infrared spectroscopy (NIRS) Results: The mean CO2 was 40±5mmHg and the mean SctO2 65±4%. Thirty-nine patients died and 43 survived (43/82 patients, 52%) until ICU discharge. The mean CO2 range during the first 24 hours after admission associated with maximal survival was 38-42mmHg (OR 2.84, 95% CI [1.15; 7.05], p=0.02). Subsequently, 2100 paired CO2/SctO2 measurements were analyzed. Based on our previous observation that the presumed ideal SctO2 is around 67%, the CO2/SctO2 scatterplot can be divided in 3 sections: (1) Hypocapnic cerebral desaturation: we found a strong linear relationship between CO2 and average SctO2 when CO2 was between 28-39mmHg (SctO2=0.50 x CO2 + 47, R2 0.76). (2) Normocapnic plateau phase: CO2’s between 40-45mmHg resulted in average SctO2’s between 66.5 and 67.5%. (3) Hypercapnic cerebral hypersaturation: we found a linear relationship between CO2 and average SctO2 when CO2 was between 46-62mmHg (SctO2=0.40 x CO2 + 47, R2 0.39). The predicted optimal CO2 (40-45mmHg) based on this physiological model corresponding with a SctO2 of 67% matched with the optimal CO2 (38-42mmHg) associated with maximal survival. Conclusion: Based on the relationship between CO2 and SctO2 and extensive survival analysis, the target CO2 in post-cardiac arrest patients seems to be 40mmHg. Since all patients received fully controlled mechanical ventilation, it is likely that there is causal relationship between iatrogenic hyperventilation/hypocapnia, cerebral desaturation and increased mortality.
Abstract Funding Acknowledgements Type of funding sources: None. Background Hemostasis in the left atrial (LA) appendage (LAA) is a common cause of stroke, particularly in atrial fibrillation (AF). LAA flow have been determined to quantify LAA function. Objectives To investigate whether LAA peak flow velocities early after cryptogenic stroke have a predictive value for AF occurrence and to determine the determinants of impaired flow. Methods Consecutive cryptogenic stroke patients (139) were enrolled. LAA flow velocities during sinus rhythm were assessed early post-stroke with transesophageal echocardiography. All patients received rhythm monitoring using 7-day Holter and if negative, an implantable cardiac monitor. Results 47 Patients (34%) developed AF during a median follow-up of 554 days, median time to AF diagnosis was 93 days. Both, LAA filling (LAAfv) and emptying (LAAev) velocities were lower in stroke patients who developed AF (resp. 44.3±14.2 cm/s and 50.7±13.3 cm/s) compared with those who didn’t (resp. 59.8±14.0 cm/s and 76.8±17.3 cm/s). LAAev was the strongest predictor of AF with an AUC of 0.878 in ROC curve analysis and with optimal cut-off value of 55 cm/s. Age and mitral regurgitation were independent determinants of reduced LAAev. Conclusions Reduced LAA flow velocities can identify cryptogenic stroke patients at high risk of occult AF, and who may benefit from intensive rhythm monitoring or anticoagulation strategies.
To use cardiac magnetic resonance (CMR) imaging with quantitative T2 mapping as surrogate for myocardial water content in patients with advanced decompensated heart failure (ADHF), compare these values with T2-values observed in chronic heart failure, and evaluate the change with decongestive therapy. Volumetric CMR measurements and quantitative T2 mapping were performed in 18 consecutive ADHF patients with clinical signs of volume overload. Eleven patients with stable heart failure were used as controls. Vasodilator therapy and diuretics were administered to achieve a pulmonary arterial wedge pressure (PAWP) of <18 mmHg and central venous pressure (CVP) of <12 mmHg, after which CMR was repeated. ADHF patients (62 ± 12 years; 89% male; left ventricular ejection fraction 23 ± 8%) presented with low cardiac index (2.08 ± 0.59 L/min/m2), high PAWP (25 ± 7 mmHg), and high CVP (14 ± 5 mmHg). After decongestion, the patients had a significant increase in cardiac index (+0.41 ± 0.53 L/min/m2; P = 0.005) and decreases in both PAWP (−9 ± 6 mmHg; P < 0.001) and CVP (−6 ± 5 mmHg; P < 0.001). At baseline, global left ventricular T2-values were higher in ADHF patients compared with controls (59.5 ± 4.6 vs. 54.7 ± 2.2 ms, respectively; P = 0.001). After decongestion, T2-values fell significantly to 55.9 ± 5.1 ms (P = 0.001), comparable with controls (P = 0.580). In contrast, psoas muscle T2-values were similar at baseline (38.6 ± 4.4 ms) vs. after decongestion (37.8 ± 4.8 ms; P = 0.397). Each 1 ms decrease in global left ventricular T2-value during decongestion was associated with a 1.14 ± 0.40 mmHg decrease in PAWP (P = 0.013), after correction for age and gender. Patients presenting with ADHF and volume overload have increased global left ventricular—but not psoas muscle—T2-values, which decrease with successful decongestion. Relief of myocardial oedema correlates with haemodynamic unloading.
Background/objectiveT2-weighted cardiovascular magnetic resonance (T2W-CMR) has shown utility in diseases such as myocarditis and tako-tsubo cardiomyopathy (TTCM) where myocardial edema may be the predominant pathological abnormality.Since these conditions may affect many myocardial regions, a more quantitative approach may help identify extent of myocardial involvement and reduce uncertainty in qualitative interpretation of T2W-CMR.We sought to evaluate the diagnostic utility of quantitative T2 mapping in patients presenting with acute myocarditis or TTCM.
To investigate whether time from onset of heart failure signs and/or symptoms (ie, progression to stage C/D heart failure) until implantation affects reverse remodelling and clinical outcome after cardiac resynchronisation therapy (CRT).
Design
Cohort study of consecutive CRT patients, implanted between 1 October 2008 and 30 April 2011.
Setting
Single tertiary care centre (Ziekenhuis Oost-Limburg, Genk, Belgium).
Patients
Consecutive CRT patients (n=172; 71±9 years), stratified into tertiles according to the time since first heart failure signs and/or symptoms at implantation.
Main outcome measures
Change in left ventricular dimensions, New York Heart Association (NYHA) functional class and freedom from all-cause mortality or heart failure admission.
Results
Baseline renal function was better in patients implanted earlier after emerging heart failure symptoms (estimated glomerular filtration rate=73±20 vs 63±23 vs 58±26 ml/min/1.73 m2 for tertiles, respectively). After 6 months, decreases in left ventricular end-diastolic/systolic diameter and improvement in NYHA functional class were similar among tertiles. Freedom from all-cause mortality or heart failure admission was better in patients with early implantation (p value=0.042). However, this was not the case in patients with preserved renal function (p value=0.794). Death from progressive heart failure was significantly more frequent in patients implanted later in their disease course.
Conclusions
Reverse left ventricular remodelling after CRT is not affected by the duration of heart failure. However, clinical outcome is better in patients implanted earlier in their disease course, which probably relates to better renal preservation.
BACKGROUND: Increased myocardial injury visualized by late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) portends worse outcomes in patients with acute coronary syndromes (ACS). Although non ST-segment acute coronary syndromes (NSTE-ACS) comprise 70% of all ACS and 1-year mortality rates are similar to the more readily-diagnosed and uniformly-treated ST-elevation myocardial infarction, ischemic changes and treatment strategies in NSTE-ACS are not well-defined, Studies have shown that T2-weighted (T2W) cardiac magnetic resonance (CMR) may be a marker of acute myocardial injury in ACS. We hypothesized that the presence of at-risk myocardium, identified by T2W CMR at presentation, predicts increased subsequent myocardial injury by LGE beyond traditional risk predictors in NSTE-ACS. METHODS & RESULTS: 48 patients enrolled in a prospective study of NSTE-ACS underwent CMR with short tau inversion recovery (T2W STIR) imaging and LGE prior to intervention and repeat CMR 61 ± 27 days later. Baseline presence/absence of increased myocardial signal intensity by T2W STIR was determined by consensus of two expert reviewers blinded to other data. In 13 patients (27%), follow-up LGE images showed more extensive injury compared to baseline. Peak troponin at time of event, baseline TIMI risk score and baseline LGE score did not predict subsequent LGE score increase (p=0.13, p=0.48, p=0.55, respectively). Conversely, a much higher proportion of patients with vs. without increased T2W STIR SI at baseline demonstrated increased myocardial injury by LGE at follow-up (12/31 vs. 1/17, p<0.01; Figure). CONCLUSION: Myocardium at-risk by T2-weighted STIR CMR in patients with NSTE-ACS predicts subsequent myocardial injury, more so than clinical predictors or extent of baseline myocardial damage. Prospective studies that intensify care for patients with at-risk myocardium may help identify strategies to improve myocardial salvage and reduce mortality in NSTE-ACS.
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