Right coronary artery diastolic perfusion pressure on outcome of patients with left heart failure and pulmonary hypertension.

AIMS: Right ventricle adaptation to prolonged exposure against pulmonary hypertension (PH) includes structural and functional abnormalities, translated into modifications of blood flow pattern through the right coronary artery. Given these changes, we investigate the relationship between right coronary artery diastolic perfusion pressure (RCDPP) and clinical outcome, in patients with PH secondary to left-sided heart failure (HF). METHODS AND RESULTS: We studied 108 HF patients who underwent right heart catheterization. PH was present in 75 (69.4%). Mean RCDPP was lower in patients with PH (59.4 ± 14.0 mmHg) as compared with no PH patients (65.5 ± 11.6 mmHg) (P = 0.03). Aortic diastolic pressure accounted for 79% of RCDPP variability explained by the model (P < 0.0001). During a median follow-up of 26 months, the RCDPP 1st tertile (<55 mmHg) [hazard ration (HR) 5.19, 95% confidence interval (CI) 1.08-25.12, P = 0.04] and left ventricular ejection fraction <45% [HR 7.26, 95% CI 1.77-29.73, P = 0.006] were independent predictors of mortality. CONCLUSIONS: Right coronary artery diastolic perfusion pressure is a strong independent haemodynamic maker of mortality in left-sided HF and PH. Excessive reduction of aortic diastolic pressure may be detrimental. Future research is necessary to determine the therapeutic approach to blood pressure in this population.

The impact of left ventricular ejection fraction on heart failure patients with pulmonary hypertension.

BACKGROUND: The most common cause of pulmonary hypertension (PH) in developed countries is left heart disease (LHD, group 2 PH). The development of PH in heart failure (HF) patients is indicative of worse outcomes. OBJECTIVE: The aim of this study was to evaluate the long term outcomes of HF patients with PH in a national long-term registry. METHODS: Study included 9 cardiology centers across Israel between 01/2013-01/2015, with a 12-month clinical follow-up and 24-month mortality follow-up. Patients were age ≥18 years old with HF and pre-inclusion PH due to left heart disease determined by echocardiography [estimated systolic pulmonary arterial pressure (SPAP) ≥ 50 mmHg]. Patients were categorized into 3 groups: HF with reduced (HFrEF < 40%), mid-range (HFmrEF 40-49%), and preserved (HFpEF ≥ 50%) ejection fraction. RESULTS: The registry included 372 patients, with high prevalence of cardiovascular risk factors. Median HF duration was 4 years and 65% were in severe HF New York Heart Association (NYHA) classification ≥3. Mean systolic pulmonary artery pressure (SPAP) was 62 ± 11 mmHg. During 2-years of follow-up, 54 patients (15%) died. Univariable predictors of mortality included NYHA grade 3-4, chronic renal failure, and SPAP ≥ 65 mmHg. Severe PH was associated with mortality in HFpEF, but not HFmrEF or HFrEF, and remained significant after multivariable adjustment with an adjusted hazard ratio of 2.99, (95%CI 1.29-6.91, p = 0.010). CONCLUSIONS: The combination of HFpEF with severe PH was independently associated with increased mortality. Currently, HFpEF patients are included with group 2 PH patients. Defining HFpEF with severe PH as a sub-class may be more appropriate, as these patients are at increased risk and deserve special consideration.

Prognostic value and diagnostic properties of the diastolic pulmonary pressure gradient in patients with pulmonary hypertension and left heart disease.

BACKGROUND: The use of the diastolic pressure gradient (DPG) for the diagnosis of combined post- and pre-capillary pulmonary hypertension (Cpc-PH) versus isolated post-capillary pulmonary hypertension (Ipc-PH) in patients with PH due to left heart disease (PH-LHD) remains controversial. We studied the incremental prognostic information provided by DPG and potential sources of disagreements between different hemodynamic criteria for Cpc-PH. METHODS: We studied 393 patients with PH-LHD who underwent right heart catheterization and were followed for hospitalizations and all-cause mortality for a median of 53 months. Patients were classified into Ipc-PH or Cpc-PH using DPG, pulmonary vascular resistance (PVR) or transpulmonary gradient (TPG)-based criteria. RESULTS: Classifying PH categories according to DPG alone was not associated with a significant difference in clinical outcomes between patients with Ipc-PH and Cpc-PH (P = 0.17). By contrast, PVR criteria alone were associated with a strong prognostic separation between Ipc-PH and Cpc-PH (P = 0.005). Adding DPG to the PVR-based classification contributed no additional prognostic information. Classifying PH using the cutoff of DPG >7 mmHg or TPG >15 mmHg, resulted in an almost perfect agreement (κ statistic 0.87; 93.4% agreement). However, in cases of disagreement, occurring with low or negative DPG values, the TPG-based classification was more likely to be correct. CONCLUSION: The DPG does not add incremental prognostic information beyond PVR. Using DPG/PVR criteria to differentiate between Ipc-PH and Cpc-PH is equivalent to using TPG/PVR criteria with a TPG threshold >15 mmHg. However, the use of DPG for diagnostic purposes may lead to misclassification of PH when DPG is low or negative.

Determinants of cardiac repolarization and risk for ventricular arrhythmias during mild therapeutic hypothermia.

PURPOSE: We aimed to investigate the factors that modulate the extent of QTc prolongation and potential arrhythmogenic consequences during mild therapeutic hypothermia (MTH). METHODS: We studied 205 patients after out-of-hospital cardiac arrest (131 underwent MTH). QTc was measured at baseline, 3h, 6h, 12h, 24h (end of hypothermia), 48h and 72h, and ventricular arrhythmias quantified. RESULTS: During MTH, the QTc interval increased progressively peaking at 12h (mean increase 42ms, 95% CI 30-55). There was a strong gender effect (P<0.001) and a significant gender-by-MTH interaction (P=0.004). At 12h, the QTc interval was markedly longer in women as compared with men (mean difference 50ms [95% CI 27-73]. Anoxic brain injury (P=0.002) was also positively associated with QTc prolongation. The risk for ventricular arrhythmic events was not higher with MTH compared with no hypothermia (incidence rate ratio 0.57, 95% CI 0.32-1.02, P=0.06). However, typical cases of Torsade de pointes occurred in association with AV block and LQT2. CONCLUSION: QTc prolongation during MTH is strongly affected by female gender and moderately by concomitant anoxic brain injury. Although the overall risk for ventricular arrhythmias is not greater with MTH, Torsade de pointes may develop when other contributing factors coexist.

Time Dependence of the Effect of Right Ventricular Dysfunction on Clinical Outcomes After Myocardial Infarction: Role of Pulmonary Hypertension.

BACKGROUND: The clinical importance of right ventricular (RV) function in acute myocardial infarction is well recognized, but the impact of concomitant pulmonary hypertension (PH) has not been studied. METHODS AND RESULTS: We studied 1044 patients with acute myocardial infarction. Patients were classified into 4 groups according to the presence or absence of RV dysfunction and PH, defined as pulmonary artery systolic pressure >35 mm Hg: normal right ventricle without PH (n=509), normal right ventricle and PH (n=373), RV dysfunction without PH (n=64), and RV dysfunction and PH (n=98). A landmark analysis of early (admission to 30 days) and late (31 days to 8 years) mortality and readmission for heart failure was performed. In the first 30 days, RV dysfunction without PH was associated with a high mortality risk (adjusted hazard ratio 5.56, 95% CI 2.05-15.09, P<0.0001 compared with normal RV and no PH). In contrast, after 30 days, mortality rates among patients with RV dysfunction were increased only when PH was also present. Compared with patients having neither RV dysfunction nor PH, the adjusted hazard ratio for mortality was 1.44 (95% CI 0.68-3.04, P=0.34) in RV dysfunction without PH and 2.52 (95% CI 1.64-3.87, P<0.0001) in RV dysfunction with PH. PH with or without RV dysfunction was associated with increased risk for heart failure. CONCLUSION: In the absence of elevated pulmonary pressures, the risk associated with RV dysfunction after acute myocardial infarction is entirely confined to the first 30 days. Beyond 30 days, PH is the stronger risk factor for long-term mortality and readmission for heart failure.

Heart failure in patients with diabetes undergoing primary percutaneous coronary intervention.

INTRODUCTION: Diabetes mellitus is associated with increased risk after acute coronary syndromes. Primary percutaneous coronary intervention is the most effective method of reperfusion for acute ST-elevation myocardial infarction and can limit the ischaemic damage to the left ventricle. However, there are few data on the impact of diabetes mellitus on the risk of heart failure following primary percutaneous coronary intervention. METHODS: We studied 958 ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention, of whom 263 (27.5%) had diabetes mellitus, with 67 (7.0%) treated with insulin. The primary end points of the study were re-admission for heart failure. Secondary end points were all-cause mortality and recurrent infarctions. The follow-up period was 5 years after hospital discharge. RESULTS: The cumulative incidence of re-admission for heart failure was 8.4%, 15.2% and 26.7% in patients without diabetes mellitus, non-insulin-treated and insulin-treated diabetes mellitus, respectively. Compared with patients without diabetes mellitus, the adjusted hazard ratio for heart failure was 1.95 (95% confidence intervals 1.30-2.93) and 3.09 (95% confidence intervals 1.71-5.60) in non-insulin-treated and insulin-treated diabetes mellitus, respectively. The corresponding hazard ratios for mortality were 1.03 (95% confidence intervals 0.68-1.55) and 2.04 (95% confidence intervals 1.22-3.42), respectively. There was a J-shaped association between fasting glucose levels in the acute phase and risk of mortality (P=0.0001) and a direct association with heart failure (P=0.03). CONCLUSION: Despite modern treatment of ST-elevation myocardial infarction and high levels of guideline-based medical care, diabetes mellitus had an independent adverse effect on the risk of re-admissions for heart failure, which was particularly high among insulin-treated patients.

Pulmonary arterial capacitance in patients with heart failure and reactive pulmonary hypertension.

AIMS: Reactive pulmonary hypertension (PH) is a severe form of PH secondary to left-sided heart failure (HF). Given the structural and functional abnormalities in the pulmonary vasculature that occur in reactive PH, we hypothesized that pulmonary artery capacitance (PAC) may be profoundly affected, with implications for clinical outcome. METHODS AND RESULTS: We studied 393 HF patients of whom 124 (32%) were classified as having passive PH and 140 (36%) as having reactive PH, and 91 patients with pulmonary arterial hypertension (PAH). Mean PAC was highest in patients without PH (4.5 ± 2.1 mL/mmHg), followed by the passive PH group (2.8 ± 1.4 mL/mmHg) and was lowest in those with reactive PH (1.8 ± 0.7 mL/mmHg) (P = 0.0001). PAC and pulmonary vascular resistance (PVR) fitted well to a hyperbolic inverse relationship (PAC = 0.25/PVR, R(2) = 0.70), with reactive PH patients dispersed almost predominantly on the flat part of the curve where a reduction in PVR is associated with a small improvement in PAC. Elevated PCWP was associated with a significant lowering of PAC for any PVR (P = 0.036). During a median follow-up of 31 months, both reactive PH [hazard ratio (HR) 2.59, 95% confidence interval (CI) 1.14-4.46, P = 0.02] and reduced PAC (HR 0.72 per 1 mL/mmHg increase, 95% CI 0.59-0.88, P = 0.001) were independent predictors of mortality. CONCLUSIONS: The development of reactive PH is associated with a marked reduction in PAC. PAC is a strong independent haemodynamic marker of mortality in HF and may contribute to the increased mortality associated with reactive PH.

Impact of functional mitral regurgitation on right ventricular function and outcome in patients with right ventricular infarction.

Right ventricular (RV) infarction is associated with increased mortality. Functional mitral regurgitation (FMR) may complicate inferoposterior infarction with RV involvement leading to pulmonary hypertension and increased RV afterload, potentially exacerbating RV remodeling and dysfunction. We studied 179 patients with inferior wall left ventricular (LV) ST-elevation myocardial infarction and RV infarction. The presence and severity of FMR and RV function were assessed by echocardiography. FMR was diagnosed based on echocardiographic criteria and when the severity of regurgitation was ≥moderate. Eighteen patients (10.0%) had ≥moderate FMR. Estimated pulmonary artery systolic pressure was higher in patients with FMR than in patients without FMR (43 ± 10 vs 34 ± 10 mmHg, respectively, p = 0.002). RV systolic dysfunction was present in 76 patients (42.5%). FMR was a strong predictor of RV dysfunction (odds ratio 5.35, 95% confidence interval [CI] 1.65 to 17.48, p = 0.005) independent of reperfusion therapy. During a median follow-up of 4.1 years, 20 (12.4%) and 10 (55.6%) deaths occurred in patients with and without FMR, respectively (p <0.001). In a multivariable Cox regression model, compared with patients without FMR and with normal RV function, the adjusted hazard ratio for mortality was 1.02 in patients without FMR and with RV dysfunction (95% CI 0.39 to 2.69, p = 0.97) and 3.62 in patients with FMR with RV dysfunction (95% CI 1.33 to 9.85, p = 0.01). In conclusion, in patients with RV infarction, the development of concomitant hemodynamically significant FMR is associated with RV dysfunction. The risk for mortality is increased predominantly in patients with both RV dysfunction and FMR.

Pulmonary hypertension, right ventricular function, and clinical outcome in acute decompensated heart failure.

BACKGROUND: Pulmonary hypertension (PH) and right ventricular (RV) dysfunction have been associated with adverse outcome in patients with chronic heart failure. However, data are lacking in the setting of acute decompensated heart failure (ADHF). We sought to determine prognostic significance of PH in patients with ADHF and its interaction with RV function. METHODS: We studied 326 patients with ADHF. Pulmonary artery systolic pressure (PASP) and RV function were determined with the use of Doppler echocardiography, with PH defined as PASP >50 mm Hg. The primary end point was all-cause mortality during 1-year follow-up. RESULTS: PH was present in 139 patients (42.6%) and RV dysfunction in 83 (25.5%). The majority of patients (70%) with RV dysfunction had PH. Compared with patients with normal RV function and without PH, the adjusted hazard ratio (HR) for mortality was 2.41 (95% confidence interval [CI] 1.44-4.03; P = .001) in patients with both RV dysfunction and PH. Patients with normal RV function and PH had an intermediate risk (adjusted HR 1.78, 95% CI 1.11-2.86; P = .016). Notably, patients with RV dysfunction without PH were not at increased risk for 1-year mortality (HR 1.04, 95% CI 0.43-2.41; P = .94). PH and RV function data resulted in a net reclassification improvement of 22.25% (95% CI 7.2%-37.8%; P = .004). CONCLUSIONS: PH and RV function provide incremental prognostic information in ADHF. The combination of PH and RV dysfunction is particularly ominous. Thus, the estimation of PASP may be warranted in the standard assessment of ADHF.

The relation between serum phosphorus levels and clinical outcomes after acute myocardial infarction.

BACKGROUND: Elevated serum phosphorus levels have been linked with cardiovascular disease and mortality with conflicting results, especially in the presence of normal renal function. METHODS: We studied the association between serum phosphorus levels and clinical outcomes in 1663 patients with acute myocardial infarction (AMI). Patients were categorized into 4 groups based on serum phosphorus levels (<2.50, 2.51-3.5, 3.51-4.50 and >4.50 mg/dL). Cox proportional-hazards models were used to examine the association between serum phosphorus and clinical outcomes after adjustment for potential confounders. RESULTS: The mean follow up was 45 months. The lowest mortality occurred in patients with serum phosphorus between 2.5-3.5 mg/dL, with a multivariable-adjusted hazard ratio of 1.24 (95% CI 0.85-1.80), 1.35 (95% CI 1.05-1.74), and 1.75 (95% CI 1.27-2.40) in patients with serum phosphorus of <2.50, 3.51-4.50 and >4.50 mg/dL, respectively. Higher phosphorus levels were also associated with increased risk of heart failure, but not the risk of myocardial infarction or stroke. The effect of elevated phosphorus was more pronounced in patients with chronic kidney disease (CKD). The hazard ratio for mortality in patients with serum phosphorus >4.5 mg/dL compared to patients with serum phosphorus 2.50-3.50 mg/dL was 2.34 (95% CI 1.55-3.54) with CKD and 1.53 (95% CI 0.87-2.69) without CKD. CONCLUSION: We found a graded, independent association between serum phosphorus and all-cause mortality and heart failure in patients after AMI. The risk for mortality appears to increase with serum phosphorus levels within the normal range and is more prominent in the presence of CKD.

Utility of pulmonary hypertension for the prediction of heart failure following acute myocardial infarction.

Pulmonary hypertension (PH) is usually perceived as a complication of established heart failure (HF) rather than as a predictor of HF or a marker of subclinical HF. PH may develop because of cardiac alterations that result in increased filling pressures after acute myocardial infarction (AMI). We hypothesized that PH might be a useful marker to predict the risk of HF after AMI. We studied 1,054 patients with AMI. Pulmonary artery systolic pressure (PASP) was estimated using echocardiography at the index admission and PH was defined as a PASP >35 mm Hg. The primary end point was readmission for HF at 1 year. PH was present in 471 patients (44.6%) and was strongly associated with age, decreased ejection fraction, advanced diastolic dysfunction, and moderate/severe mitral regurgitation (p <0.0001 for all comparisons). Area under the receiver operating characteristic curve was significantly higher for estimated PASP (0.74 ± 0.02) compared to other echocardiographic parameters (p = 0.02 to 0.0003). After adjustments for clinical and echocardiographic variables in a Cox model, PH was associated with a hazard ratio of 3.10 for HF (95% confidence interval 1.31 to 2.57, p <0.0001). After adding estimated PASP to a model containing clinical and echocardiographic risk factors, net reclassification improvement was 0.21 (95% confidence interval 0.11 to 0.31, p <0.0001). In conclusion, PASP integrates the severity of multiple hemodynamic determinants of increased left atrial pressures that lead to an increase in pulmonary venous pressure. In AMI, PH at the index admission is a useful marker in unmasking latent subclinical HF and predicting the development of overt HF.

Relationship between reactive pulmonary hypertension and mortality in patients with acute decompensated heart failure.

BACKGROUND: In patients with heart failure, pulmonary hypertension (PH) predicts higher risk for morbidity and mortality. However, few data are available on the prognostic implications of reactive (precapillary) PH superimposed on passive (postcapillary) PH. METHODS AND RESULTS: We performed a subgroup analysis of 242 patients with acute decompensated heart failure assigned to pulmonary artery catheter placement in the Vasodilation in the Management of Acute Congestive Heart Failure trial. Patients were classified into 3 groups, using the final (posttreatment) hemodynamic measurements: (1) no PH (mean pulmonary artery pressure ≤ 25 mm Hg; (2) passive PH (mean pulmonary artery pressure > 25, pulmonary capillary wedge pressure >15 mm Hg, and pulmonary vascular resistance ≤ [corrected] Wood units); and (3) reactive PH (mean pulmonary artery pressure > 25, [corrected] pulmonary capillary wedge pressure >15 mm Hg, and pulmonary vascular resistance > 3 Wood units). Fifty-eight patients were classified as normal mean pulmonary artery pressure, 124 with passive PH and 60 with reactive PH. During follow-up of 6 months, 5 (8.6%), 27 (21.8%), and 29 (48.3%) deaths occurred in patients without PH, patients with passive PH, and with reactive PH, respectively (P<0.0001). After multivariable adjustments, reactive PH remained an independent predictor of death, with an adjusted hazard ratio of 4.8 compared with patients without PH, and 2.8 compared with patients with passive PH (95% confidence interval, 1.7 to 4.7, P=0.0001). Similar results were obtained when reactive PH was defined on the basis of transpulmonary gradient. CONCLUSIONS: Reactive PH is common among patients with acute decompensated heart failure after initial diuretic and vasodilator therapy. The adverse outcome associated with PH is predominantly due to increased mortality rates in the subgroup of patients with reactive PH.

Angiographically uncertain left main coronary artery narrowings: correlation with multidetector computed tomography and intravascular ultrasound.

BACKGROUND: Angiographic assessment of left main coronary artery (LMCA) stenosis is often difficult and unreliable. To date, intravascular ultrasound (IVUS) is used to determine the significance of lesions in patients with LMCA stenosis of uncertain significance. We aimed to prospectively show the ability of multidetector computed tomography (MDCT) to assess LMCA luminal and plaque dimensions, and to characterize atherosclerotic plaque, as compared to IVUS and quantitative coronary angiography (QCA), in patients with angiographically uncertain LMCA stenosis. METHODS: Twenty patients, with angiographically uncertain LMCA stenosis, underwent coronary evaluation with IVUS, QCA and 16-slice MDCT. Minimal lumen diameter (MLD), minimal lumen area (MLA), lumen area stenosis (LAS) and plaque burden (PB) were assessed. RESULTS: The MLD (median [interquartile range]) was 3.2 mm (2.5-3.7) by IVUS, 2.8 mm (2.3-3.3) by QCA (r=0.52, P<0.05), and 2.8 mm (2.5-3.8) by MDCT (r=0.77, P<0.01). MDCT estimated MLA as 10.7 mm(2) (7.1-12.6) Vs. 9.9 mm(2) (6.5-13.5) by IVUS (r=0.93, P<0.01). Very high correlations were observed between MDCT and IVUS in assessing LAS (mean +/- SD) (25.8+/-19.1% and 29.0+/-24.9% respectively, r=0.83, P<0.01), and PB (49.2+/-15.8% and 49.2+/-19.7% respectively, r=0.94, P<0.01). MDCT assigned plaque as being non-calcified with a sensitivity of 100%, while calcified plaques with a sensitivity of 75%. CONCLUSION: A high degree of correlation was found between MDCT and IVUS regarding the assessment of minimal lumen diameter and area, lumen area stenosis and plaque burden as well as plaque characterization in patients with angiographically borderline LMCA stenosis. Therefore, in patients selected for non-invasive coronary tree evaluation, MDCT may provide a valuable tool for the assessment, decision-making and follow-up of patients with uncertain LMCA disease.

Predictive value of white blood cell subtypes for long-term outcome following myocardial infarction.

INTRODUCTION: Elevation of total white blood cells (WBC) count is associated with higher mortality in patients with acute coronary syndromes. However, it is unknown which specific subset of leukocytes best correlates with increased risk of adverse outcome. METHODS AND RESULTS: We prospectively studied the predictive value of WBC subtypes for long-term outcome in 1037 patients with acute myocardial infarction (AMI). Total WBC, neutrophil, monocyte and lymphocyte counts, and high-sensitivity C-reactive protein (CRP) were obtained in each patient. The median duration of follow up was 23 months (range, 6-42 months). Analyzed separately, baseline total WBC (HR 2.2, 95% CI 1.5-3.3; P<0.0001), neutrophil (HR 2.7, 95% CI 1.8-4.1; P<0.0001) and monocyte (HR 1.9, 95% CI 1.3-2.8; P=0.001) counts in the upper quartile, and lymphocyte count in the lower quartile (HR 1.5, 95% CI 1.1-2.3; P=0.03), were all independent predictors of mortality. Comparing nested models, adding other WBC data failed to improve model based on neutrophil count. In contrast, adding neutrophil count to the models based on total WBC (P=0.01), on monocyte count (P<0.0001) or on lymphocyte count (P<0.0001) improved the prediction of the models. Neutrophil count in the upper quartile (>or=9800 microL(-1)) remained a strong independent predictor of mortality after adjustment for left ventricular systolic function and for CRP (HR 2.2, 95% CI 1.6-3.0; P<0.0001). CONCLUSION: Of all WBC subtypes, elevated neutrophil count best correlates with mortality in patients with AMI. Neutrophil count provides additive prognostic information when combined with CRP.

Diagnostic accuracy of myocardial hypoenhancement on multidetector computed tomography in identifying myocardial infarction in patients admitted with acute chest pain syndrome.

OBJECTIVE: To evaluate prevalence and diagnostic accuracy of myocardial hypoenhancement (MH) using multidetector computed tomography (MDCT) in patients admitted for acute chest pain syndromes. METHODS: Sixty-nine patients underwent first-pass MDCT, coronary angiography, and echocardiography. Using a standardized analysis protocol, left ventricular short-axis reformations were evaluated for presence, size, and density of MH in 16 myocardial segments. These were correlated with the presence and location of myocardial infarction (MI), regional myocardial dysfunction, and coronary artery disease. RESULTS: Myocardial hypoenhancement was found in acute MI (27/35), healed MI (6/14), unstable angina (3/9), and atypical chest pain (0/11). Sensitivity, specificity, and positive and negative predictive values of MH for diagnosing any MI were 67%, 85%, 92% and 52%, respectively. CONCLUSIONS: The presence of MH on MDCT in acute chest pain patients has high positive predictive value and specificity but only moderate sensitivity for presence of acute or healed MI using the strict criteria proposed in this study.

Is functional improvement after myocardial infarction predicted with myocardial enhancement patterns at multidetector CT?

PURPOSE: To prospectively evaluate the sensitivity of myocardial early perfusion defects (EDs) and late enhancement (LE) at multidetector computed tomography (CT) following acute myocardial infarction (AMI) to predict segment myocardial dysfunction and myocardial functional recovery (MFR), by using echocardiography as the reference standard. MATERIALS AND METHODS: Institutional review board approval and informed consent were obtained. Twenty-six patients (25 men, one woman; mean age, 53 years+/-9 [standard deviation]), underwent baseline multidetector CT, coronary angiography, and echocardiography within a week of AMI and a follow-up echocardiography at 3 months. ED, LE, and late hypoattenuation were compared with regional left ventricular function and MFR. A logistic regression model and generalized estimating equation analysis were applied to estimate the predictive effect of ED and LE. Differences between groups were evaluated by using nonpaired Student t tests. RESULTS: All EDs and LE corresponded with AMI location determined by using angiography and echocardiography. For occluded arteries (n=5), no relationship was found between the presence of ED or LE and MFR. For patent arteries (n=21), presence of LE had a respective sensitivity and specificity of 73% and 85% for predicting follow-up segment dysfunction, compared with 57% and 90% for ED. In abnormal baseline segments, nonrecovery was clearly related to the presence and size of segment defect area for both ED (odds ratio: 1.95 [95% confidence interval: 0.9, 4.1] per square centimeter) and LE (odds ratio: 1.85 [95% confidence interval: 1.2, 2.9] per square centimeter). Segments that recovered had significantly lower prevalence of ED and LE, and if present, were significantly smaller than in segments remaining abnormal (P<.05). CONCLUSION: The presence and size of ED and LE at multidetector CT is closely related to follow-up segment myocardial dysfunction and MFR.

Primary percutaneous coronary intervention after out-of-hospital cardiac arrest: patients and outcomes.

BACKGROUND: The decision to perform primary percutaneous coronary intervention in unconscious patients resuscitated after out-of-hospital cardiac arrest is challenging because of uncertainty regarding the prognosis of recovery of anoxic brain damage and difficulties in interpreting ST segment deviations. In ST elevation myocardial infarction patients after OHCA, primary PCI is generally considered the only option for reperfusion. There are few published studies and no randomized trial has yet been performed in this specific group of patients. OBJECTIVES: To define the demographic, clinical and angiographic characteristics, and the prognosis of STEMI patients undergoing primary PCI after out-of-hospital cardiac arrest. METHODS: We performed a retrospective analysis of medical records and used the prospectively acquired information from the Rambam Primary Angioplasty Registry (PARR) and the Rambam Intensive Cardiac Care (RICCa) databases. RESULTS: During the period March 1998 to June 2006, 25 STEMI patients (21 men and 4 women, mean age 56 +/- 11years) after OHCA were treated with primary PCI. The location of myocardial infarction was anterior in 13 patients (52%) and non-anterior in 12 (48%). Cardiac arrest was witnessed in 23 patients (92%), but bystander resuscitation was performed in only 2 patients (8%). Eighteen patients (72%) were unconscious on admission, and Glasgow Coma Scale > 5 was noted in 2 patients (8%). Cardiogenic shock on admission was diagnosed in 4 patients (16%). PCI procedure was successful in 22 patients (88%). In-hospital, 30 day, 6 month and 1 year survival was 76%, 76%, 76% and 72%, respectively. In-hospital, 30 day, 6 month and 1 year survival without severe neurological disability was 68%, 68%, 68% and 64%, respectively. CONCLUSIONS: In a selected group of STEMI patients after out-of-hospital cardiac arrest, primary PCI can be performed with a high success rate and provides reasonably good results in terms of short and longer term survival.