Gonzalo Barge-Caballero

Prevalencia, causas y pronóstico de las «falsas alarmas» al laboratorio de hemodinámica en pacientes con sospecha de infarto de miocardio con elevación del segmento ST

Introduccion y objetivos. Determinar prevalencia, causas y pronostico de las «falsas alarmas» al laboratorio de hemodinamica (FALH) en una red regional de angioplastia primaria. Metodos. Registro prospectivo de 1.662 pacientes remitidos para angioplastia primaria entre enero de 2003 y agosto de 2008. Se definio FALH como ausencia de lesion coronaria causal. Resultados. En 120 pacientes (7,2%; intervalo de confianza [IC] del 95%, 5,9-8,5) no se identifico ninguna lesion coronaria causal. De ellos, 104 (6,3%; IC del 95%, 5,1-7,4) recibieron un diagnostico alternativo a IAMCEST, 91 (5,5%; IC del 95%, 4,3-6,6) no presentaron enfermedad coronaria significativa y 64 (3,8%; IC del 95%, 2,9-4,8) presentaron marcadores de dano miocardico negativos. Los diagnosticos alternativos mas frecuentes fueron: infarto con onda Q previo (18 casos), alteraciones inespecificas del segmento ST (11), pericarditis (10) y discinesia apical transitoria (10). La mortalidad a 30 dias fue similar en los pacientes con y sin lesion causal (el 5,8 frente al 5,8%; p = 0,99). La prevalencia de FALH fue discretamente superior entre los pacientes remitidos desde los servicios de urgencias de hospitales no intervencionistas sin evaluacion previa por un cardiologo que entre los remitidos por cardiologos desde el servicio de urgencias del hospital intervencionista (el 9,5 frente al 6,1%; p = 0,02; odds ratio [OR] = 1,64; IC del 95%, 1,08-2,5). No observamos un exceso de FALH entre los pacientes remitidos por medicos de UVI Moviles-061 (7,2%; p = 0,51; OR = 1,37; IC del 95%, 0,79-2,37). Conclusiones. Hemos observado una prevalencia de FALH del 7,2% de acuerdo con el criterio de ausencia de lesion coronaria causal. Nuestros resultados indican que diferentes modelos de activacion del laboratorio de hemodinamica podrian justificar discretas variaciones en la prevalencia de FALH.

Prevalence, etiology, and outcome of catheterization laboratory false alarms in patients with suspected ST-elevation myocardial infarction

INTRODUCTION AND OBJECTIVES To investigate the prevalence, causes and outcome of catheterization laboratory false alarms (CLFAs) in a regional primary angioplasty network. METHODS A prospective registry of 1,662 patients referred for primary angioplasty between January 2003 and August 2008 was reviewed to identify CLFAs (i.e. when no culprit coronary lesion could be found). RESULTS No culprit coronary lesion could be identified in 120 patients (7.2%; 95% confidence interval [CI], 5.9-8.5%). Of these, 104 (6.3%, 95% CI, 5.1-7.4%) had a discharge diagnosis other than ST-elevation myocardial infarction, 91 (5.5%; 95% CI, 4.3-6.6%) had no significant coronary disease, and 64 (3.8%; 95% CI, 2.9-4.8%) tested negative for cardiac biomarkers. The most frequent alternative diagnoses were: previous Q-wave myocardial infarction (18 cases), nonspecific ST-segment abnormalities (11), pericarditis (10) and transient apical dyskinesia (10). The 30-day mortality rate was similar in patients with and without culprit lesions (5.8% vs. 5.8%; P=.99). The prevalence of CLFAs was slightly higher in patients not previously evaluated by a cardiologist and referred from emergency departments in hospitals without catheterization laboratories than in those referred by cardiologists from emergency departments at hospitals with such facilities (9.5% vs. 6.1%; P=.02; odds ratio=1.64; 95% CI, 1.08-2.5). The prevalence of CLFAs was not significantly higher in patients referred by physicians with out-of-hospital emergency medical services (7.2%; P=.51; odds ratio=1.37; 95% CI, 0.79-2.37). CONCLUSIONS The prevalence of CLFAs was 7.2%, with the criterion of no culprit coronary lesion. Our findings suggest that different patterns of referral to catheterization laboratories could account for small variations in the prevalence of CLFAs.

Impact of electrocardiographic interpretability on outcome in patients referred for stress testing.

Eur J Clin Invest 2012; 42 (5): 541–547

Late graft failure in heart transplant recipients: incidence, risk factors and clinical outcomes.

To analyse the incidence, risk factors and clinical outcomes of late graft failure after heart transplantation.

Prognostic Value of the Nutritional Risk Index in Heart Transplant Recipients

INTRODUCTION AND OBJECTIVES To study the prognostic impact of preoperative nutritional status, as assessed through the nutritional risk index (NRI), on postoperative outcomes after heart transplantation (HT). METHODS We conducted a retrospective, single-center study of 574 patients who underwent HT from 1991 to 2014. Preoperative NRI was calculated as 1.519 × serum albumin (g/L) + 41.7 × (body weight [kg] / ideal body weight [kg]). The association between preoperative NRI and postoperative outcomes was analyzed by means of multivariable logistic regression and multivariable Cox regression. RESULTS Mean NRI before HT was 100.9 ± 9.9. According to this parameter, the prevalence of severe nutritional risk (NRI < 83.5), moderate nutritional risk (83.5 ≤ NRI < 97.5), and mild nutritional risk (97.5 ≤ NRI < 100) was 5%, 22%, and 10%, respectively. One year post-transplant mortality rates in these 4 categories were 18.2%, 25.3%, 7.9% and 10.2% (P < .001), respectively. The NRI was independently associated with a lower risk of postoperative infection (adjusted OR, 0.97; 95%CI, 0.95-1.00; P = .027) and prolonged postoperative ventilator support (adjusted OR, 0.96; 95%CI, 0.94-0.98; P = .001). Patients at moderate or severe nutritional risk had significantly higher 1-year post-HT mortality (adjusted HR, 1.55; 95%CI, 1.22-1.97; P < .001). CONCLUSIONS Malnourished patients have a higher risk of postoperative complications and mortality after HT. Preoperative NRI determination may help to identify HT candidates who might benefit from nutritional intervention.

Acute coronary artery occlusions complicating a valve-in-valve-in-valve procedure

An 83-year-old female with prior 23-mm Mitroflow biological prosthetic aortic valve replacement (Sorin Group Inc, Mitroflow Division, Vancouver, Canada), symptomatic severe periprosthetic regurgitation and preserved left ventricular ejection fraction was referred for transcatheter aortic valve implantation (TAVI). Preprocedural catheterisation showed normal coronary arteries and severe aortic regurgitation. Although TAVI is licensed for treating native valve aortic stenosis it can be used off label for treating bio-prosthetic valve failure due to aortic regurgitation. A 23-mm Edwards SAPIEN transcatheter aortic prosthetic valve (Edwards Lifesciences, Irvine, California, USA) via right femoral artery was deployed. Due to persistence of severe …

Noninvasive monitoring of acute and chronic rejection in heart transplantation.

Purpose of review Recent years have seen advances in the early detection of cardiac graft rejection. Recent findings We review the possibilities offered by tissue Doppler imaging and speckle tracking echocardiography, cardiac magnetic resonance, cardiac computed tomography, single positron emission tomography, gene expression profiling, and quantitation of donor-derived cell-free DNA, and microRNAs. Summary Noninvasive monitoring of acute and chronic rejection after cardiac transplantation is an unmet need and remains a challenge. Imaging techniques and peripheral blood biomarkers are the most commonly used approaches, and in recent years there has been great progress. Gene expression profiling seems to be useful for ruling out the presence of a moderate to severe acute cellular rejection in stable, low-risk patients. Newer monitoring tools, like donor-derived cell-free DNA or microRNA, seem to be promising for individualizing immunosuppressive therapies and better understanding the mechanisms of rejection.

Prognostic Significance of Heart Rate and its Long-term Trend in Cardiac Transplant Patients

INTRODUCTION AND OBJECTIVES The aim of the present study was to examine the prognostic significance of heart rate and its trend in heart transplantation. METHODS This observational study enrolled 170 patients who received a bicaval heart transplant between 1995 and 2005; all were in sinus rhythm. The resting heart rate was determined via electrocardiography at the end of the first posttransplant year and annually until the tenth year. Cox analysis was used to evaluate the incidence of adverse events with a mean (standard deviation) follow-up of 8.9 (3.1) years. The primary study end point was the composite outcome of death or graft dysfunction. RESULTS The resting heart rate at the end of the first posttransplant year was an independent predictor of the primary composite end point (hazard ratio=1.054; 95% confidence interval, 1.028-1.080; P<.001) and was significantly associated with total mortality (hazard ratio=1.058; 95% confidence interval, 1.030-1.087; P<.001) and mortality from cardiac causes (hazard ratio=1.069; 95% confidence interval, 1.026-1.113; P=.001), but not with graft dysfunction (hazard ratio=1.028; 95% confidence interval, 0.989-1.069; P=.161). For patients with a heart rate ≥ 105 or<90 bpm vs those with 90-104 bpm, the hazard ratios of the primary end point were 2.233 (95% confidence interval, 1.250-3.989; P=.007) and 0.380 (95% confidence interval, 0.161-0.895; P=.027), respectively. Heart rate tended to decrease in the first 10 years after transplantation (P=.001). Patients with a net increase in heart rate during follow-up showed a higher incidence of adverse events. CONCLUSIONS An elevated heart rate is an adverse prognostic marker after heart transplantation.

Clinical evaluation of rosuvastatin in heart transplant patients with hypercholesterolemia and therapeutic failure of other statin regimens: short‐term and long‐term efficacy and safety results

We conducted an observational study of 30 heart transplant recipients with serum low‐density lipoprotein cholesterol (LDL‐c) >100 mg/dl despite previous statin therapy, who were treated with rosuvastatin 10 mg daily (5 mg in case of renal dysfunction). Serum lipids, creatine phosphokinase (CPK), bilirubin, and hepatic enzymes were prospectively measured 2, 4, and 12 weeks after the initiation of the drug. Clinical outcomes of patients who continued on long‐term rosuvastatin therapy beyond this 12‐week period were reviewed in February 2015. Over the 12‐week period following rosuvastatin initiation, serum levels of total cholesterol (TC) and LDL‐c and the ratio TC/high‐density lipoprotein cholesterol (HDL‐c) decreased steadily (P < 0.001). Average absolute reductions of these three parameters were –48.7 mg/dl, –46.6 mg/dl, and –0.9, respectively. Seventeen (57%) achieved a serum LDL‐c < 100 mg/dl. No significant changes from baseline were observed in serum levels of triglycerides, HDL‐c, hepatic enzymes, bilirubin, or CPK. Twenty‐seven (90%) patients continued on long‐term therapy with rosuvastatin over a median period of 3.6 years, with no further significant variation in lipid profile. The drug was suspended due to liver toxicity in 1 (3.3%) patient and due to muscle toxicity in 2 (6.7%) patients. All adverse reactions resolved rapidly after rosuvastatin withdrawal. Our study supports rosuvastatin as a reasonable alternative for heart transplant recipients with hypercholesterolemia and therapeutic failure of other statin regimens.

Left ventricular torsion during exercise in patients with and without ischemic response to exercise echocardiography.

INTRODUCTION AND OBJECTIVES Left ventricular torsion decreases during transmural myocardial ischemia, but the effect of exercise on left ventricular torsion has not been widely studied. We hypothesized that exercise-induced ischemia may impair left ventricular torsion. Therefore, our aim was to study the effects of exercise on left ventricular torsion in patients with an ischemic response to exercise echocardiography and in patients with a normal response. METHODS A retrospective analysis was performed in 172 patients with ejection fraction ≥ 50% who were referred for exercise-echocardiography and studied by speckle imaging at rest, peak and postexercise. Torsion was defined as apical rotation - basal rotation (in degrees) / left ventricular length (in centimeters). A total of 114 patients had a normal exercise echocardiography and 58 patients had an ischemic response to exercise echocardiography. RESULTS Patients with ischemic response to the test exhibited less basal rotation at peak exercise (+0.30° [2.39°] vs -0.65° [2.61°] in the normal group; P = .03), whereas peak apical rotation was similar (ischemic response to the test, 7.80° [3.51°]; normal response, 7.27° [3.28°]; P =.36). Torsion at peak exercise was also similar (1.07° [0.60°] in the ischemic response to the test group vs 1.16° [0.57°] in normal group; P =.37). A more impaired peak basal rotation was found in patients with anterior or anterior+posterior involvement (anterior ischemic response, +1.22° [2.45°]; anterior + posterior ischemic response, -0.20° [2.25°]; posterior ischemic response, -0.71° [1.96°]; normal response, -0.65° [2.60°]; P =.02). CONCLUSIONS Basal rotation at peak exercise is impaired in patients with an ischemic response to exercise echocardiography, particularly in those with anterior involvement. Apical rotation and torsion are similar to those in patients with normal exercise echocardiography.