Transvenous removal of cardiac implantable electronic device leads.

INTRODUCTION AND OBJECTIVE: The number and complexity of cardiac implantable electronic devices (CIEDs) have increased, as has the number of related complications, often leading to removal of the implanted system. The aim of this study was to characterize transvenous explantation/extraction of CIED leads in a reference center. METHODS: This was a descriptive observational study of patients consecutively admitted from January 2009 to May 2014 for transvenous lead extraction. RESULTS: The sample consisted of 109 patients, with a mean age of 64.6±16.62 years, 73.1% male. The main indication for lead extraction was CIED infection. The mean time from first implantation to lead removal was 5.6±4.89 years. Blood cultures were positive in 32.8% of cases and 29% of patients had vegetations on echocardiography. A total of 228 cardiac leads were removed, of which 58.8% were ventricular, 32.4% atrial and 8.8% coronary sinus. Complete clinical success was achieved in 97.2% of cases, while procedural success was complete in 93.4% and partial in 5.3%. The complications reported were three cases of significant pocket hematoma, one of subclavian vein thrombosis and three of cardiac tamponade, effectively treated by pericardiocentesis. CONCLUSIONS: Transvenous explantion or extraction of CIED leads was highly effective. A high level of experience is an essential factor in the success and safety of the procedure.

Endothelial progenitor cells in diabetic patients with myocardial infarction - can statins improve their function?

The effect of statins on endothelial progenitor cells (EPCs) function derived from diabetic patients (DMpts) with acute myocardial infarction (AMI) is unknown. In this study we assess the response of early and late EPCs from diabetic versus non-diabetic patients (NDMpts) with AMI to statins. EPCs were obtained from 10 diabetic and 10 age-matched non-diabetic male patients with AMI. For each patient, cultures of early and late EPCs were performed under 4 different conditions: normal glucose concentration (control); high glucose concentration; normal glucose concentration with atorvastatin supplementation and normal glucose concentration with pravastatin supplementation. To compare the effect of these treatments on EPC function in DMpts versus NDMpts, we performed in vitro: EPC colony-forming units (CFU) assay; cell cycle analysis; viability assessment and expression of the surface markers CXCR4, CD133, CD34 and KDR. Under control conditions, CFU numbers were reduced in DMpts-derived EPCs when compared to those of NDMpts (1.4±0.8 vs 2.6±1.2 CFU/well, P=0.021). When early EPCs from DMpts were cultured in the presence of statins, CFU capacity was restored, surmounting that of NDMpts under control conditions. Statins significantly improved viability of early EPCs and delayed the onset of late EPCs senescence, even in cells from DMpts. In addition, statins induced approximately a 2-fold increase in the proportion of late EPCs in S-phase of the cell cycle (P<0.05). Statins have a beneficial effect on both early and late EPCs from DMpts with AMI. Despite the functional impairment of EPCs from DMpts, they exhibit similar responsiveness to statins as equivalent cells from NDMpts.

Impact of prior chronic statin therapy and high-intensity statin therapy at discharge on circulating endothelial progenitor cell levels in patients with acute myocardial infarction: a prospective observational study.

BACKGROUND: Endothelial progenitor stem cells (EPCs) are mobilized to the peripheral circulation in response to myocardial ischemia, playing a crucial role in vascular repair. Statins have been shown to stimulate EPCs. However, neither the impact of previous statin therapy on EPC response of acute myocardial infarction (AMI) patients nor the effect of post-AMI high-intensity statin therapy on the evolution of circulating EPC levels has yet been addressed. Therefore, we aimed to compare circulating EPC levels between patients receiving long-term statin therapy before the AMI and statin-naive patients and to assess the impact of high-intensity statin therapy at discharge on the evolution of circulating EPCs post-AMI. METHODS: This is a prospective observational study of 100 AMI patients. Circulating EPCs (CD45dimCD34 + KDR + cells) and their subpopulation coexpressing the homing marker CXCR4 were quantified by the high-performance flow cytometer FACSCanto II in whole blood, in two different moments: within the first 24 h of admission and 3 months post-AMI. Patients were followed up clinically for 2 years. RESULTS: Patients previously treated with statins had significantly higher levels of EPCs coexpressing CXCR4 (1.9 ± 1.4 vs. 1.3 ± 1.0 cells/1,000,000 events, p = 0.031) than statin-naive patients. In addition, the subanalysis of diabetics (N = 38) also revealed that patients previously on statins had significantly greater numbers of both CD45dimCD34 + KDR + CXCR4+ cells (p = 0.024) and CD45dimCD34 + KDR + CD133+ cells (p = 0.022) than statin-naive patients. Regarding the evolution of EPC levels after the AMI, patients not on a high-intensity statin therapy at discharge had a significant reduction of CD45dimCD34 + KDR + and CD45dimCD34 + KDR + CXCR4+ cells from baseline to 3 months follow-up (p = 0.031 and p = 0.005, respectively). However, patients discharged on a high-intensity statin therapy maintained circulating levels of all EPC populations, presenting at 3 months of follow-up significantly higher EPC levels than patients not on an intensive statin therapy. Moreover, the high-intensity statin treatment group had significantly better clinical outcomes during the 2-year follow-up period than patients not discharged on a high-intensity statin therapy. CONCLUSION: Chronic statin therapy prior to an AMI strongly enhances the response of EPCs to myocardial ischemia, even in diabetic patients. Furthermore, high-intensity statin therapy after an AMI prevents the expected decrease of circulating EPC levels during follow-up. These results reinforce the importance of an early and intensive statin therapy in AMI patients.

Reduced levels of circulating endothelial progenitor cells in acute myocardial infarction patients with diabetes or pre-diabetes: accompanying the glycemic continuum.

BACKGROUND: Diabetic patients have a significantly worse prognosis after an acute myocardial infarction (AMI) than their counterparts. Previous studies have shown that the number of circulating endothelial progenitor cells (EPCs) significantly increase early after an AMI in normoglycemic patients. However, it is well known that type 2 diabetes mellitus (DM) is associated with impaired function and reduced circulating EPCs levels. Nonetheless, few studies have analyzed EPCs response of diabetics to an AMI and the EPC response of pre-diabetic patients has not been reported yet. Therefore, we hypothesized that in the acute phase of an AMI, diabetic and pre-diabetics have lower circulating EPCs levels than patients with normal glucose metabolism. We also evaluated the possible capacity of chronic antidiabetic treatment in the recovery of EPCs response to an AMI in diabetics. METHODS: One-hundred AMI patients were prospectively enrolled in the study. Using the high-performance flow cytometer FACSCanto II, circulating EPCs (CD45dimCD34+KDR+ and CD45dimCD133+KDR+ cells) were quantified, within the first 24 hours of admission. In addition, as an indirect functional parameter, we also analyzed the fraction of EPCs coexpressing the homing marker CXCR4. RESULTS: We found that in the acute phase of an AMI, diabetic patients presented significantly lower levels of circulating CD45dimCD34+KDR+ and CD45dimCD133+KDR+ EPCs by comparison with nondiabetics, with a parallel decrease in the subpopulations CXCR4+ (p < 0.001). Indeed, this study suggests that the impaired response of EPCs to an AMI is an early event in the natural history of DM, being present even in pre-diabetes. Our results, also demonstrated that numbers of all EPCs populations were inversely correlated with HbA1c (r = -0.432, p < 0.001 for CD45dimCD34+KDR+ cells). Finally, this study suggests that previous chronic insulin therapy (but not oral antidiabetic drugs) attenuate the deficient response of diabetic EPCs to an AMI. CONCLUSION: This study indicates that there is a progressive decrease in EPCs levels, from pre-diabetes to DM, in AMI patients. Moreover, glycemic control seems to be determinant for circulating EPCs levels presented in the acute phase of an AMI and chronic insulin therapy may probably attenuate the deficit in EPCs pool seen in diabetics.

Circulating endothelial progenitor cells as a predictor of response to cardiac resynchronization therapy: the missing piece of the puzzle?

BACKGROUND: It would be important to better identify heart failure (HF) patients most likely to respond to cardiac resynchronization therapy (CRT). Because endothelial progenitor cells (EPCs) play a crucial role in the maintenance of vascular endothelium integrity, we hypothesize that patients who have higher circulating EPCs levels have greater neovascularization potential and are more prone to be responders to CRT. METHODS: Prospective study of 30 consecutive patients, scheduled for CRT. Echocardiographic evaluation was performed before implant and 6 months after. Responders to CRT were defined as patients who were still alive, have not been hospitalized for HF management, and demonstrated ≥15% reduction in left ventricular end-systolic volume (LVESV) at the 6-month follow-up. EPCs were quantified before CRT, from peripheral blood, by flow cytometry using five different conjugated antibodies: anti-CD34, anti-KDR, anti-CD133, anti-CD45, and anti-CXCR4. We quantified five different populations of angiogenic cells: CD133(+) /CD34(+) cells, CD133(+) /KDR(+) cells, CD133(+) /CD34(+) /KDR(+) cells, CD45(dim) CD34(+) /KDR(+) cells, and CD45(dim) CD34(+) /KDR(+) /CXCR4(+) cells. RESULTS: The proportion of responders to CRT at the 6-month follow-up was 46.7%. Responders to CRT presented higher baseline EPCs levels than nonresponders (0.0003 ± 0.0006% vs 0.0001 ± 0.0002%, P = 0.04, for CD34(+) /CD133(+) /KDR(+) and 0.0006 ± 0.0005% vs 0.0003 ± 0.0003%, P = 0.009, for CD45(dim) CD34(+) /KDR(+) /CXCR4(+) cells). In addition, baseline levels of CD45(dim) CD34(+) /KDR(+) /CXCR4(+) cells were positively correlated with the reduction of LVESV verified 6 months after CRT (r = 0.497, P = 0.008). CONCLUSIONS: High circulating EPCs levels may identify the subset of HF patients who are more likely to undergo reverse remodeling and benefit from CRT. Addition of EPCs levels assessment to current selection criteria may improve the ability to predict CRT response.

Predictors of pulmonary hypertension after intermediate-to-high risk pulmonary embolism.

BACKGROUND: Pulmonary embolism (PE) is a common cardiovascular emergency that, when combined with chronic thromboembolic pulmonary hypertension (PH), is associated with high mortality and morbidity. We aimed to determine the incidence of and predisposing factors for the development of PH after a PE episode. METHODS: A retrospective study was conducted in 213 patients admitted to an intensive care unit with intermediate-to-high risk PE between 2000 and 2010. Clinical data at admission were collected and the incidence of PH as assessed by echocardiography (estimated pulmonary systolic artery pressure over 40 mmHg) was determined. Multivariate analysis was used to determine predictors of development of PH. RESULTS: PH was detected in 12.4% of patients after a mean follow-up of three years. Only age (hazard ratio [HR] 1.09, 95% confidence interval [CI] 1.02-1.20 per year; p=0.012) and body mass index (HR 1.19, 95% CI 1.04-1.36) per kg/m2, p=0.013) emerged as independent predictors of the development of this complication during follow-up. CONCLUSIONS: PH after PE was a relatively common complication in our series. We identified advanced age and increased body mass index as predisposing factors.

Added value of cardiac magnetic resonance in etiological diagnosis of ventricular arrhythmias.

INTRODUCTION: Cardiac magnetic resonance (CMR) imaging is increasingly important in the diagnostic work-up of a wide range of heart diseases, including those with arrhythmogenic potential. OBJECTIVE: To assess the added value of CMR in etiological diagnosis of ventricular arrhythmias after an inconclusive conventional investigation. METHODS: Patients undergoing CMR between 2005 and 2011 for investigation of ventricular arrhythmias were included (n=113). All had documented arrhythmias. Those with a definite diagnosis from a previous investigation and those with evidence of coronary artery disease (acute coronary syndrome, typical angina symptoms, increase in biomarkers or positive stress test) were excluded. CMR results were considered relevant when they fulfilled diagnostic criteria. RESULTS: Of the 113 patients, 57.5% were male and mean age was 41.7 ± 16.2 years. Regarding the initial arrhythmia, 38.1% had ventricular fibrillation/sustained ventricular tachycardia (VF/VT) and 61.9% had less complex ventricular ectopy. CMR imaging showed criteria of a specific diagnosis in 42.5% of patients, was totally normal in 36.3%, and showed non-specific alterations in the remainder. In VF/VT patients, specific criteria were found in 60.4%, and in 31.4% of those with less complex ectopy. The most frequent diagnoses were arrhythmogenic right ventricular dysplasia, ventricular non-compaction and myopericarditis. It is worth noting that, although there was no evidence of previous coronary artery disease, 6.2% of patients had a late gadolinium enhancement distribution pattern compatible with myocardial infarction. CONCLUSION: CMR gives additional and important information in the diagnostic work-up of ventricular arrhythmias after an inconclusive initial investigation. The proportion of patients with diagnostic criteria was 42.5% (60.0% in those with VF/VT), and CMR was completely normal in 36.6%.

Left ventricular mechanical dyssynchrony in patients with impaired left ventricular function undergoing gated SPECT myocardial perfusion imaging.

INTRODUCTION: Gated SPECT myocardial perfusion imaging (MPI) has been used to quantify mechanical dyssynchrony. Mechanical dyssynchrony appears to be related to response to cardiac resynchronization therapy. OBJECTIVE: To evaluate the presence and predictors of mechanical dyssynchrony in patients with impaired left ventricular function (LVEF) ≤50%. METHODS: The study included 143 consecutive patients referred for gated SPECT MPI with LVEF ≤50%. Gated SPECT MPI was performed according to a stress/rest protocol acquiring images with Tc 99m-tetrofosmin. Emory Cardiac Toolbox software was used for phase analysis and a standard deviation (SD) ≥43° was considered to indicate mechanical dyssynchrony. RESULTS: Mechanical dyssynchrony was present in 53.1% of the patients. Its predictors were diabetes (OR 2.0, p≤0.05), summed stress score (OR 1.1, p≤0.0005), summed rest score (OR 1.1, p≤0.0001), end-diastolic volume (OR 1.0, p≤0.0001), LVEF (OR 0.9, p≤0.0001), LVEF ≤35% (OR 3.1, p≤0.005) and LVEF ≤35% and QRS ≥120 ms (OR 3.5, p≤0.05). In this study QRS width and QRS ≥120 ms were not predictors of mechanical dyssynchrony. CONCLUSIONS: Myocardial perfusion imaging can be used to assess mechanical dyssynchrony. In patients with impaired ventricular function mechanical dyssynchrony was highly prevalent and was related to parameters of left ventricular function and perfusion.

CHADS(2) and CHA(2)DS(2)VASc scores as predictors of cardioembolic sources in secondary stroke prevention.

INTRODUCTION AND OBJECTIVES: Cardioembolism is one of the most common causes of ischemic stroke, with an estimated prevalence of 20-30%, and correct diagnosis is essential given the therapeutic implications. Although stroke risk scores (CHADS2 and more recently CHA2DS2-VASc) have been validated in heterogeneous populations of patients with atrial fibrillation, their accuracy has not been ascertained for secondary stroke prevention. We set out to assess the sensitivity and specificity of the CHADS2 and CHA2DS2-VASc stroke risk scores as predictors of cardioembolic sources, documented by transesophageal echocardiography (TEE) in a population with ischemic stroke. METHODS: The CHADS2 and CHA2DS2-VASc scores were applied to all patients admitted to the stroke unit/neurology ward of a Portuguese tertiary hospital with atrial fibrillation (diagnosed previously or during or after admission) who underwent TEE between January and August 2011. The presence of a cardioembolic source was defined as the observation by TEE of spontaneous echo contrast in the left atrium and atrial appendage or thrombi in the left cardiac chambers. RESULTS: We studied 94 patients, 66.0% male, mean age 64.4 years (standard deviation 14.2). A cardioembolic source was detected in 20 patients. ROC curve analysis identified as predictors of cardioembolic source CHADS2 score ≥4 (sensitivity of 75.0%, specificity of 66.0%, p=0.014) and CHA2DS2-VASc score ≥5 (sensitivity of 83.3%, specificity of 58.0%, p=0.009). CONCLUSIONS: Both scores showed acceptable sensitivity as predictors of embolic risk in the context of secondary prevention of cardioembolic stroke. The CHA2DS2-VASc score has higher sensitivity than CHADS2 but lower specificity.

Suspected coronary artery disease and myocardial infarction with normal coronary angiography: a heterogeneous but benign condition?

INTRODUCTION: Previous follow-up studies of patients with symptoms and/or non-invasive tests suggestive of ischemia or an acute coronary syndrome and a normal coronary angiogram have reported a good prognosis. OBJECTIVES: The aim of this study was to evaluate the clinical characteristics and outcome of a cohort of patients with suspected ischemic heart disease and normal coronary arteries. METHODS: A clinical follow-up was performed of 607 patients (mean age 62±11 years) with symptoms or non-invasive tests suggestive of ischemia (544) or myocardial infarction (63) and normal coronary angiography. The occurrence of major cardiac events or of readmission due to chest pain was recorded during a mean follow-up of 33.6±9.5 months after angiography. RESULTS: Patients with myocardial infarction were older (65.4±11.1 vs. 61.9±10.7, p=0.05), and the majority were women (68.3%). Hypertension was reported by 65.5% of patients, diabetes by 17.9%, dyslipidemia by 58.6%, smoking by 14% and family history of coronary artery disease in 11%. During follow-up no patient died from cardiovascular causes; three patients (0.5%) suffered myocardial infarction and 50 (8.3%) had recurrent chest pain leading to emergency admission. Patients with myocardial infarction had more events (20.6%) than those referred for angiography due to symptoms and/or positive non-invasive tests for ischemia (7.4%) (log-rank chi-square test: 13.6, p<0.0005). CONCLUSION: The incidence of risk factors was high. Our data suggest that patients with a normal angiogram had a good prognosis in spite of their baseline clinical presentation. A significant number of patients showed persistence of symptoms.

Digoxin in advanced heart failure patients: a question of rhythm.

BACKGROUND: The impact of digoxin on outcomes of patients with advanced heart failure (HF) remains uncertain and its effect may be different for patients in atrial fibrillation (AF) or sinus rhythm (SR). OBJECTIVES: To determine the impact of digoxin on outcomes of advanced HF patients and to assess whether prognosis differs in patients in AF and SR. METHODS: A total of 268 consecutive patients admitted to an intensive care unit with decompensated HF were evaluated. Patients were divided into two groups: A - patients with AF (n=89), and B - patients in SR (n=179). For each group we compared patients medicated and not medicated with digoxin. A mean follow-up of 3.3 years was performed. RESULTS: Addition of digoxin to contemporary standard HF therapy showed no impact on mortality of patients in group B (all-cause mortality in follow-up: 19.1% vs. 22.5%, p=0.788). Regarding group A, we observed significantly lower medium-term mortality for patients on digoxin therapy (18.6% vs. 46.6%, p=0.048). Digoxin therapy did not influence readmissions for decompensated HF. Among AF patients, no differences were found regarding demographic, clinical, echocardiographic and laboratory variables between patients medicated and not medicated with digoxin. CONCLUSIONS: Digoxin therapy may improve the prognosis of advanced HF patients with AF under optimal medical therapy. However, no benefit of digoxin was demonstrated for patients in SR. These results may help to improve patient selection for digoxin therapy.

Effect of vorapaxar on myocardial infarction in the thrombin receptor antagonist for clinical event reduction in acute coronary syndrome (TRA·CER) trial.

AIMS: The TRA·CER trial compared vorapaxar, a novel platelet protease-activated receptor (PAR)-1 antagonist, with placebo in 12 944 patients with high-risk non-ST-segment elevation acute coronary syndromes (NSTE ACS). In this analysis, we explored the effect of vorapaxar on myocardial infarction (MI). METHODS AND RESULTS: A blinded, independent central endpoint adjudication committee prospectively defined and classified MI according to the universal MI definition, including peak cardiac marker value (creatine kinase-MB [CK-MB] and/or troponin). Because the trial failed to meet its primary endpoint, these analyses are considered exploratory. During a median follow-up of 502 days, 1580 MIs occurred in 1319 patients. The majority (n = 1025, 64.9%) were type 1 (spontaneous) MI, followed by type 4a [percutaneous coronary intervention (PCI)-related] MI (n = 352; 22.3%). Compared with placebo, vorapaxar reduced the hazard of a first MI of any type by 12% [hazard ratio (HR), 0.88; 95% confidence interval (CI), 0.79-0.98; P = 0.021] and the hazard of total number of MIs (first and subsequent) by 14% (HR, 0.86; 95% CI, 0.77-0.97; P = 0.014), an effect that was sustained over time. Vorapaxar reduced type 1 MI by 17% (HR, 0.83; 95% CI, 0.73-0.95; P = 0.007). Type 4a MIs were not significantly reduced by vorapaxar (HR, 0.90; 95% CI, 0.73-1.12; P = 0.35). Vorapaxar effect was consistent across MI sizes defined by peak cardiac marker elevations and across key clinical subgroups; however, in patients not treated with thienopyridine at baseline (HR, 0.65; 95% CI, 0.46-0.92) compared with patients who received thienopyridine (HR, 0.91; 95% CI, 0.81-1.02), there was a trend towards a higher effect (Pint = 0.077). CONCLUSION: The PAR-1 antagonist vorapaxar was associated with a reduction of MI, including total number of infarctions. This reduction was sustained over time and was mostly evident in type 1 MI, the most common type of MI observed.

Long-term effect of bosentan in pulmonary hypertension associated with complex congenital heart disease.

BACKGROUND: Bosentan is recommended for symptomatic patients with Eisenmenger syndrome due to simple congenital lesions such as atrial and ventricular septal defects (VSD). However, its long-term efficacy and safety in patients with pulmonary arterial hypertension (PAH) associated with complex congenital heart disease (CHD) is unknown. OBJECTIVES: We examined the short- and long-term effects and safety profile of bosentan in patients with PAH and complex CHD. METHODS: We followed 14 patients with PAH and complex CHD for a mean of four years. Demographic parameters, exercise capacity assessed by the six-minute walking test (6MWT) and oxygen saturation were assessed at baseline, six months and at follow-up. RESULTS: Mean age was 37.1 ± 11.7 years; 90% were in WHO class III or IV. The most common diagnosis was pulmonary atresia with VSD (35.7%), followed by truncus arteriosus (28.6%), patent ductus arteriosus (21.4%) and transposition of the great arteries (14.3%). After six months of treatment, six-minute walking distance (6MWD) increased from 371.9 to 428.4 m (p=0.005) and functional class was improved (p=0.005). After four years, one patient discontinued bosentan due to side effects and four patients were started on sildenafil, after a mean 38 months of bosentan treatment. Mean 6MWD for patients on bosentan monotherapy (n=8) was 440.1 ± 103.8 m, whereas for patients on bosentan-sildenafil combination therapy (n=4) it was 428.8 ± 96.9 m, after four years of therapy. Two patients died during follow-up. CONCLUSIONS: Bosentan was safe and was associated with improved exercise capacity in patients with PAH and complex CHD. This improvement was sustained for up to four years and the safety profile was similar to simple CHD patients.

Circumferential ascending aortic strain and aortic stenosis.

BACKGROUND: Two-dimensional speckle tracking (2D-ST) echocardiography for the measurement of circumferential ascending thoracic aortic strain (CAAS) in the context of aortic stenosis (AS) is not elucidated. Purpose This study assesses the thoracic ascending aortic deformation using 2D-ST echocardiography in AS patients. Population and methods Forty-five consecutive patients with an aortic valvular area (AVA) ≤0.85 cm(2)/m(2) were included. Regarding aortic deformation, the global peak CAAS was the parameter used, and an average of six segments of arterial wall deformation was calculated. The corrected CAAS was calculated as the global CAAS/pulse pressure (PP). Aortic stiffness (ß2) index was assessed according to ln(Ps/Pd)/CAAS. The sample was stratified according to the stroke volume index (SVI) as: Group A (low flow, SVI ≤35 mL/m(2); n = 19) and Group B (normal flow, SVI >35 mL/m(2); n = 26). RESULTS: The mean age was 76.8 ± 10.3 years, 53.3% were male, the mean indexed AVA was 0.43 ± 0.15 cm(2)/m(2), and the mean CAAS was 6.3 ± 3.0%. The CAAS was predicted by SVI (ß = 0.31, P < 0.01) and by valvulo-arterial impedance (Zva). The corrected CAAS was correlated with the M-mode guided aortic stiffness index (ß1) (r = -0.39, P < 0.01), and was predicted by SVI, Zva, and systemic arterial compliance (ß = 0.15, P < 0.01). The ß2 index was significantly higher for the low-flow patients (16.1 ± 4.8 vs. 9.8 ± 5.3, P < 0.01), and was predicted by SVI (ß -0.58, P < 0.01) and PP (ß = 0.17, P < 0.01). Global CAAS was more accurate to predict low flow than Zva, systolic function and systemic vascular resistance. CONCLUSION: In patients with moderate-to-severe aortic stenosis, SVI and LV afterload-related variables were the most important determinants of 2S-ST global CAAS.

[Cardiac magnetic resonance stress perfusion: a single-center study]. / Ressonância magnética cardíaca de perfusão em stress: a experiência de um centro nacional.

INTRODUCTION AND OBJECTIVES: Myocardial ischemia can be assessed with cardiac magnetic resonance perfusion imaging (MRPI). This study aimed to analyze the clinical utility of MRPI in the diagnosis of significant coronary artery disease. METHODS: Fifty-five patients were examined with a 1.5 T MR scanner (Siemens Symphony), with a first pass of 0.10 mmol/kg gadolinium chelate, at rest and during adenosine vasodilatation (140µg/kg/min for 4min) using an inversion recovery steady-state free precession sequence. The results were compared with coronary angiography and with SPECT myocardial perfusion images. Agreement for qualitative diagnosis was measured by the kappa coefficient, taking statistical significance as 95%. Minimum clinical follow-up was 12 months. RESULTS: In 19 patients (34.5%) MRPI was negative for myocardial ischemia and necrosis, in 17 (30.9%) it was negative for ischemia but positive for necrosis, in 7 (12.7%) only ischemia was present and in 12 (21.8%) the ischemic area was larger than the necrotic area. The correlation between MRPI and coronary angiography for ischemia detection by coronary artery territory was very good: left anterior descending and right coronary - k=0.8571 (0.59-1), circumflex - k=0.8108 (0.59-1). By contrast, there was no correlation in terms of myocardial ischemia detection between MRPI and SPECT. CONCLUSIONS: MRPI is able to diagnose significant coronary disease in a high risk population, by detection of myocardial ischemia.

One-shot diagnostic and prognostic assessment in intermediate- to high-risk acute pulmonary embolism: the role of multidetector computed tomography.

INTRODUCTION: Contrast-enhanced multidetector computed tomography (MDCT) is useful for the diagnosis of pulmonary embolism (PE). However, current guidelines do not support its use for risk assessment in acute PE patients. OBJECTIVES: We compared the prognostic impact of MDCT-derived indices regarding medium-term mortality in a population of intermediate- to high-risk PE patients, mostly treated by thrombolysis. METHODS: Thirty-nine consecutive patients admitted to an intensive care unit with acute PE were studied. All patients had a pulmonary MDCT on admission to the emergency room as part of the diagnostic algorithm. We assessed the following MDCT variables: right ventricular/left ventricular diameter (RV/LV) ratio, arterial obstruction index, pulmonary artery-to-aorta diameter ratio and azygos vein diameter. A 33-month follow-up was performed. RESULTS: Mean age was 59.1±19.6 years, with 80% of patients receiving thrombolysis. Follow-up all-cause mortality was 12.8%. Of the MDCT-derived variables, only the RV/LV ratio had significant predictive value, being higher in patients who suffered the endpoint (1.6±0.5 vs. 1.9±0.4, p=0.046). Patients with an RV/LV ratio ≥1.8 had 11-fold higher medium-term all-cause mortality (3.8% vs. 38.8%, p<0.001). Regarding this endpoint, the c-statistic was 0.78 (95% CI, 0.60-0.96) for RV/LV ratio and calibration was good (goodness-of-fit p=0.594). No other radiological index was predictive of mortality. CONCLUSIONS: MDCT gives the possibility, in a single imaging procedure, of diagnosing and assessing the prognosis of patients with intermediate- to high-risk PE. Although further studies are needed, the simple-to-calculate RV/LV ratio has good discrimination and calibration for predicting poorer outcomes in patients with acute PE.

Renal artery aneurysm: an endovascular treatment for a rare cause of hypertension.

Renal artery aneurysms are a rare cause of secondary hypertension. Endovascular treatment with a polytetrafluoroethylene (PTFE)-coated stent can exclude aneurysms and treat hypertension. We report the case of a 23-year-old man with hypertension diagnosed three years earlier and in whom renal angiography revealed three aneurysms involving the right renal artery. A covered stent was implanted, resulting in successful exclusion of the aneurysm. Ten months after the procedure the patient is asymptomatic and with normal blood pressure without antihypertensive therapy.

Platelet aggregation at discharge: a useful tool in acute coronary syndromes?

INTRODUCTION: Inhibition of platelet aggregation appears two hours after the first dose of clopidogrel, becomes significant after the second dose, and progresses to a steady-state value of 55% by day seven. Low response to clopidogrel has been associated with increased risk of stent thrombosis and ischemic events, particularly in the context of stable heart disease treated by percutaneous coronary intervention. OBJECTIVE: To stratify medium-term prognosis of an acute coronary syndrome (ACS) population by platelet aggregation. METHODS: We performed a prospective longitudinal study of 70 patients admitted for an ACS between May and August 2009. Platelet function was assessed by ADP-induced platelet aggregation using a commercially available kit (Multiplate(®) analyzer) at discharge. The primary endpoint was a combined outcome of mortality, non-fatal myocardial infarction, or unstable angina, with a median follow-up of 136.0 (79.0-188.0) days. RESULTS: The median value of platelet aggregation was 16.0U (11.0-22.5U) with a maximum of 41.0U and a minimum of 4.0U (normal value according to the manufacturer: 53-122U). After ROC curve analysis with respect to the combined endpoint (AUC 0.72), we concluded that a value of 18.5U conferred a sensitivity of 75.0% and a specificity of 68% to that result. We therefore created two groups based on that level: group A - platelet aggregation <18.5U, n=44; and group B - platelet aggregation ≥18.5U, n=26. The groups were similar with respect to demographic data (age 60.5 [49.0-65.0] vs. 62.0 [49.0-65.0] years, p=0.21), previous cardiovascular history, and admission diagnosis. There were no associations between left ventricular ejection fraction, GRACE risk score, or length of hospital stay and platelet aggregation. The groups were also similar with respect to antiplatelet, anticoagulant, proton pump inhibitor (63.6 vs. 46.2%, p=0.15) and statin therapy. The variability in platelets and hemoglobin was also similar between groups. Combined event-free survival was higher in group A (96.0 vs. 76.7%, log-rank p<0.01). Platelet aggregation higher than 18.5U was an independent predictor of the combined event (HR 6.75, 95% CI 1.38-32.90, p=0.02). CONCLUSION: In our ACS population platelet aggregation at discharge was a predictor of medium-term prognosis.

[Fulminant myocarditis]. / Miocardite fulminante - a propósito de um caso clínico.

A 46-year-old woman was admitted due to diplopia because of ophthalmoplegia, which improved with corticosteroid therapy. Eight days later, she was admitted with fulminant myocarditis in cardiogenic shock, with severe left ventricular dysfunction and frequent episodes of nonsustained ventricular tachycardia. As there was no clinical improvement, an endomyocardial biopsy was performed that revealed inflammatory infiltrate, vasculitis, and PCR positive for cytomegalovirus, Epstein-Barr virus, parvovirus B19 and enterovirus. Left ventricular function recovered with heart failure treatment and corticosteroids. Three months later, after progressive withdrawal of prednisolone, there was recurrence of myocarditis and left ventricular dysfunction, which was successfully treated by restarting corticosteroid therapy. One month later she was readmitted with fulminant myocarditis which again responded to steroids. She intermittently presented cutaneous purpura lesions. At this time the provisional diagnosis was vasculitis and she started monthly cycles of cyclophosphamide. Before the second cycle she was admitted with pneumonia and ventricular dysfunction and died.