Luiz Pereira de Magalhães

Anti-inflammatory effect of atorvastatin (80 mg) in unstable angina pectoris and non–Q-wave acute myocardial infarction

In this randomized trial, C-reactive protein increased during the first 5 days of an acute coronary syndrome in patients treated with placebo, but this phenomenon was not observed in those randomized to atorvastatin 80 mg/day. This suggests that short-term statin therapy inhibits inflammation in patients with non-ST-elevation acute coronary syndromes.

Clinical, electrocardiographic, and electrophysiologic characteristics of patients with a fasciculoventricular pathway: The role of PRKAG2 mutation

BACKGROUND The ECG, clinical, and electrophysiologic profiles of patients with a fasciculoventricular pathway are well described. Fasciculoventricular pathways occurring in the setting of glycogen storage cardiomyopathy possess unique features. OBJECTIVE The purpose of this study was to compare the clinical, ECG, and electrophysiologic characteristics of patients with a fasciculoventricular pathway, with or without glycogen storage cardiomyopathy. METHODS Two groups of patients with a fasciculoventricular pathway were compared: group A consisted of 10 patients with the PRKAG2 mutation (Arg302gln), and group B consisted of 9 patients without the mutation. RESULTS Thirty percent of group A patients had left ventricular hypertrophy, and none had an additional accessory pathway. Group B patients had no structural heart disease, and 33% had an additional accessory pathway. Group A patients had a slower resting heart rate (56 ± 7 vs 75 ± 10 bpm, P <0.0001), a wider QRS complex (0.15 ± 0.01 vs 0.11 ± 0.02 ms, P = .0004), and a longer HV interval (34 ± 1 vs 25 ± 3 ms, P = .0003). During long-term follow-up, 50% of group A patients developed complete AV block versus none in group B. Eighty percent of group A patients developed atrial flutter and/or atrial fibrillation. No Group B patient had any arrhythmia during follow-up after successful ablation of additional arrhythmia circuits. No sustained ventricular arrhythmia was induced in any patient from either group. CONCLUSION Patients with a fasciculoventricular pathway associated with the PRKAG2 mutation have distinct clinical, ECG, and electrophysiologic profiles and should be correctly identified because of their ominous long-term prognosis. Patients without the mutation have an excellent arrhythmia-free prognosis after treatment of additional circuits.

Familial Pseudo-Wolff-Parkinson-White Syndrome

Introduction: PRKAG2 plays a role in regulating metabolic pathways, and mutations in this gene are associated with familial ventricular preexcitation, hypertrophic cardiomyopathy, and atrioventricular conduction disturbances. Clinico‐pathologic and experimental data suggest the hypothesis of a glycogen storage disease.

Prevalence and prognostic value of ventricular dyssynchrony in chagas cardiomyopathy

BACKGROUND: Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE: Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS: 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION: Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.BACKGROUND Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction < 45% in the echocardiogram. The echocardiogram evaluated the presence of intraventricular dyssynchrony using 3 criteria and interventricular dyssynchrony using 1 criterion. Patients were followed for 21 ± 14 months and cardiac events were defined as the combination of death and hospitalization. RESULTS The average age of the population was 56 ± 10 years, 50% males. Mean ejection fraction was 30 ± 8% and 87% presented functional class I/II (NYHA). The prevalence of interventricular dyssynchrony was 34% (95% CI: 22%-48%) and intraventricular dyssynchrony had a prevalence of 85% (95% CI: 75%-93%). The prevalence of intraventricular dyssynchrony was similar among patients with QRS duration < 0.12 s or > 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.

Effect of atorvastatin (80 mg) on recurrent ischemia in unstable angina pectoris or Non–ST-Elevation acute myocardial infarction

A body of evidence has suggested that many cellular actions of statin therapy may acutely improve endothelial function even before affecting the lipid profile.1 Statins can acutely enhance nitric oxide bioavailability via their lipid-independent actions by upregulating endothelial nitric oxide synthase.2 In this randomized clinical trial, we evaluated the effect of high-dose atorvastatin on myocardial ischemia measured by ST-segment monitoring during the first 2 days after an episode of unstable angina pectoris (UAP) or non–Q-wave acute myocardial infarction (AMI). • • • Patients admitted to the coronary care unit of Portuguese Hospital, Salvador, Brazil, due to UAP or non–Q-wave AMI from December 2000 to March 2002 were considered candidates for the study. Inclusion criteria were defined as onset of chest discomfort in the previous 48 hours in patients with electrocardiographic changes consisting of transient ST-segment depression ( 0.05 mV), T-wave inversion ( 0.1 mV) and/or positive troponin I ( 1.0 ng/dl). Patients with positive troponin results were defined as having AMI, otherwise they were characterized as UAP. Patients were excluded if they had left bundle branch block, any liver disease, history of statin intolerance, pregnancy, or lactation. The study was approved by the local ethic committee and all participants provided written informed consent. A first blood sample to measure plasma lipids was drawn before initiation of therapy. The enrolled patients were submitted to a randomized, double-blind, placebo-controlled program with either 80 mg of atorvastatin or placebo administered once a day. ST-segment recording (Holter) was performed during the first 2 days of therapy and treatment efficacy was primarily assessed by comparing the amount of ischemia measured by Holter in the 2 groups. After 5 days, experimental therapy was withdrawn and another blood sample was taken for evaluation of the drug effect on plasma lipids. Cardiovascular events during hospitalization, defined as the composite of death, nonfatal AMI, and recurrent UAP, were also recorded. No other type of lipid-lowering therapy was offered to the patients during the first 5 days. Continuous 2-channel electrocardiographic recordings was performed by a calibrated amplitude-modulated cassette recorder (Dynamis 3000, Sao Paulo, Brazil) to detect reversible ST-segment shifts compatible with ischemia, which was defined as a 0.1 mV ST-segment depression or elevation measured 80 ms after the J point, lasting 1 minute and separated by the last episode by 1 minute. Number of ischemic episodes and total ischemia duration was measured in each patient. Ischemic burden was defined as the product of ischemic duration in minutes by the ST-segment depression in millimeters.3 The time from the first episode of ischemia was also recorded. Commercial enzymatic methods were used for the determination of total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides (Dimension Clinical Chemistry System; Dade-Behring, Newark, Delaware).4 HDL cholesterol was determined by the same method used for total cholesterol after precipitation of apolipoprotein B containing lipoproteins with magnesium phosphotungstate. Low-density lipoprotein (LDL) cholesterol was calculated by Friedewald’s formula. Duration of ischemia, number of ischemic epidodes, ischemic burden, and time to the first ischemic episode in each patient were compared between the 2 groups by Wilcoxon’s rank-sum test. The prevalence of patients with ischemia and of patients with 60 minutes of ischemia were compared between the 2 groups by Fisher’s exact test. Baseline characteristics were compared by unpaired Student’s t test for continuous variables and by chi-square or Fisher’s exact tests for categorical variables. Wilcoxon’s sign-rank test was utilized for the paired analysis of plasma lipid changes after therapy in each group. Cardiovascular events were compared between the 2 groups by the chi-square test. Nonparametric tests were applied in most situations because Holter variables were not normally distributed. Analysis of variance and logistic regression were utilized to adjust Holter variables to baseline differences between the groups. We calculated a sample size of 50 patients per group, based on a 2-sided of 5% and a statistical power of 85%, assuming that a 50% reduction in duration of ischemia with atorvastatin would be clinically significant. We based this calculation on the previously described 11 9 minutes of ischemia per patient with UAP per 24 hours.5 One hundred patients were randomized (64 12 years; 51 men); 55 had AMI and 45 had UAP. Fifty From the School of Medicine, Federal University of Bahia, Salvador; Cardiology Division, Portuguese Hospital, Salvador; and Heart Institute (InCor), University of Sao Paulo Medicine School, Sao Paulo, Brazil. Dr. Correia’s address is: Rua do Taruma 90/1002, Salvador BA, Brazil 41.810-440. E-mail: lucorrei@terra.com.br. Manuscript received November 22, 2002; revised manuscript received and accepted February 24, 2003.

Prevalência e valor prognóstico da dissincronia ventricular na cardiomiopatia chagásica

BACKGROUND: Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE: Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS: 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION: Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.BACKGROUND Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction < 45% in the echocardiogram. The echocardiogram evaluated the presence of intraventricular dyssynchrony using 3 criteria and interventricular dyssynchrony using 1 criterion. Patients were followed for 21 ± 14 months and cardiac events were defined as the combination of death and hospitalization. RESULTS The average age of the population was 56 ± 10 years, 50% males. Mean ejection fraction was 30 ± 8% and 87% presented functional class I/II (NYHA). The prevalence of interventricular dyssynchrony was 34% (95% CI: 22%-48%) and intraventricular dyssynchrony had a prevalence of 85% (95% CI: 75%-93%). The prevalence of intraventricular dyssynchrony was similar among patients with QRS duration < 0.12 s or > 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.

Delayed right ventricular perforation in patient with implantable cardioverter - defibrillator.

We describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.Palabras clave Desfibriladores implantáveis, ruptura do septo ventricular, eletrodos implantáveis. Describimos un caso de una mujer de 62 años que regresó para evaluación nueve meses después de implantación de un desfibrilador cardiaco implantable (DCI) con signos de perforación tardía del ventrículo derecho. Se discuten los signos clínicos que permitan el diagnóstico de esta presentación tardía, así como el comportamiento y la frecuencia de esta complicación en la literatura. Perforación tardía de VD en Portador de DCIWe describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.

Prevalencia y valor pronóstico de la disincronía ventricular en la miocardiopatía chagásic

BACKGROUND: Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE: Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS: 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION: Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.BACKGROUND Chagas cardiomyopathy is one important cause of heart failure in Latin America. Ventricular dyssynchrony may be a factor of decompensation in the course of this disease, but there are no data on its prevalence and its main prognostic implications yet. OBJECTIVE Describe prevalence and prognostic value of ventricular dyssynchrony in Chagas cardiomyopathy. METHODS 56 patients with Chagas cardiomyopathy were consecutively selected by two positive serologies and an ejection fraction < 45% in the echocardiogram. The echocardiogram evaluated the presence of intraventricular dyssynchrony using 3 criteria and interventricular dyssynchrony using 1 criterion. Patients were followed for 21 ± 14 months and cardiac events were defined as the combination of death and hospitalization. RESULTS The average age of the population was 56 ± 10 years, 50% males. Mean ejection fraction was 30 ± 8% and 87% presented functional class I/II (NYHA). The prevalence of interventricular dyssynchrony was 34% (95% CI: 22%-48%) and intraventricular dyssynchrony had a prevalence of 85% (95% CI: 75%-93%). The prevalence of intraventricular dyssynchrony was similar among patients with QRS duration < 0.12 s or > 0.12 s (85% and 89%, respectively, p = 0.66). Twenty events were recorded. The incidence of combined events was similar in patients with or without intraventricular dyssynchrony (35% versus 38%, p = 0.9) and those with or without interventricular dyssynchrony (39% versus 34%, p = 0.73). CONCLUSION Patients with Chagas cardiomyopathy have high intraventricular and moderate interventricular prevalence of dyssynchrony. The high prevalence is independent from the QRS width. The ventricular dyssynchrony does not have any prognostic value in patients with Chagas cardiomyopathy.

Perforación tardía de VD en portador de DCI

We describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.Palabras clave Desfibriladores implantáveis, ruptura do septo ventricular, eletrodos implantáveis. Describimos un caso de una mujer de 62 años que regresó para evaluación nueve meses después de implantación de un desfibrilador cardiaco implantable (DCI) con signos de perforación tardía del ventrículo derecho. Se discuten los signos clínicos que permitan el diagnóstico de esta presentación tardía, así como el comportamiento y la frecuencia de esta complicación en la literatura. Perforación tardía de VD en Portador de DCIWe describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.

Perfuração tardia de ventrículo direito em portador de cardioversor desfibrilador implantável

We describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.Palabras clave Desfibriladores implantáveis, ruptura do septo ventricular, eletrodos implantáveis. Describimos un caso de una mujer de 62 años que regresó para evaluación nueve meses después de implantación de un desfibrilador cardiaco implantable (DCI) con signos de perforación tardía del ventrículo derecho. Se discuten los signos clínicos que permitan el diagnóstico de esta presentación tardía, así como el comportamiento y la frecuencia de esta complicación en la literatura. Perforación tardía de VD en Portador de DCIWe describe the case of a 62-year-old patient who returned for evaluation nine months after receiving an implantable cardioverter-defibrillator (ICD) with signs of delayed right ventricular (RV) perforation. The clinical signs that allowed the diagnosis of this late presentation to be achieved are discussed herein, as well as the conduct and the frequency of this complication in the literature.