Assessment of the cardiovascular effects of electroconvulsive therapy in individuals older than 50 years.

To evaluate the impact of electroconvulsive therapy on arterial blood pressure, heart rate, heart rate variability, and the occurrence of ischemia or arrhythmias, 38 (18 men) depressive patients free from systemic diseases, 50 to 83 years old (mean: 64.7 +/- 8.6) underwent electroconvulsive therapy. All patients were studied with simultaneous 24-h ambulatory blood pressure and Holter monitoring, starting 18 h before and continuing for 3 h after electroconvulsive therapy. Blood pressure, heart rate, heart rate variability, arrhythmias, and ischemic episodes were recorded. Before each session of electroconvulsive therapy, blood pressure and heart rate were in the normal range; supraventricular ectopic beats occurred in all patients and ventricular ectopic beats in 27/38; 2 patients had non-sustained ventricular tachycardia. After shock, systolic, mean and diastolic blood pressure increased 29, 25, and 24% (P < 0.001), respectively, and returned to baseline values within 1 h. Maximum, mean and minimum heart rate increased 56, 52, and 49% (P < 0.001), respectively, followed by a significant decrease within 5 min; heart rate gradually increased again thereafter and remained elevated for 1 h. Analysis of heart rate variability showed increased sympathetic activity during shock with a decrease in both sympathetic and parasympathetic drive afterwards. No serious adverse effects occurred; electroconvulsive therapy did not trigger any malignant arrhythmias or ischemia. In middle-aged and elderly people free from systemic diseases, electroconvulsive therapy caused transitory increases in blood pressure and heart rate and a decrease in heart rate variability but these changes were not associated with serious adverse clinical events.

Assessment of the cardiovascular effects of electroconvulsive therapy in individuals older than 50 years

To evaluate the impact of electroconvulsive therapy on arterial blood pressure, heart rate, heart rate variability, and the occurrence of ischemia or arrhythmias, 38 (18 men) depressive patients free from systemic diseases, 50 to 83 years old (mean: 64.7 ± 8.6) underwent electroconvulsive therapy. All patients were studied with simultaneous 24-h ambulatory blood pressure and Holter monitoring, starting 18 h before and continuing for 3 h after electroconvulsive therapy. Blood pressure, heart rate, heart rate variability, arrhythmias, and ischemic episodes were recorded. Before each session of electroconvulsive therapy, blood pressure and heart rate were in the normal range; supraventricular ectopic beats occurred in all patients and ventricular ectopic beats in 27/38; 2 patients had non-sustained ventricular tachycardia. After shock, systolic, mean and diastolic blood pressure increased 29, 25, and 24 percent (P < 0.001), respectively, and returned to baseline values within 1 h. Maximum, mean and minimum heart rate increased 56, 52, and 49 percent (P < 0.001), respectively, followed by a significant decrease within 5 min; heart rate gradually increased again thereafter and remained elevated for 1 h. Analysis of heart rate variability showed increased sympathetic activity during shock with a decrease in both sympathetic and parasympathetic drive afterwards. No serious adverse effects occurred; electroconvulsive therapy did not trigger any malignant arrhythmias or ischemia. In middle-aged and elderly people free from systemic diseases, electroconvulsive therapy caused transitory increases in blood pressure and heart rate and a decrease in heart rate variability but these changes were not associated with serious adverse clinical events.

Sinus bradycardia as a predictor of right coronary artery occlusion in patients with inferior myocardial infarction.

Differentiation of right coronary artery (RCA) from left circumflex artery (LCxA) occlusion may be difficult since both can present an electrocardiographic pattern of inferior myocardial infarction (IMI). We studied 133 patients with IMI, 92 patients with RCA occlusion and 41 patients with LCxA occlusion. Risk factors such as previous MI, arterial hypertension, diabetes, smoking, and dislipemia, were similar for RCA and LCxA occlusions. Patients with RCA occlusion had a higher incidence of isolated IMI than patients with LCxA occlusion, 50% vs. 17%, respectively (P<0.001). Arterial hypotension was more prevalent (P<0.05) among patients with RCA (18%) rather than those with LCxA occlusion (2%). RCA occlusion presented an association with sinus bradycardia, an association not observed with LCxA occlusion (15% vs. 0%, respectively; P<0.01). Total atrioventricular block was only present among patients with RCA (18%). Proximal occlusions of the RCA presented lower heart rates (sinus bradycardia) than medial and distal occlusions (13% vs. 1% and 1%, respectively; P<0.0001 and P<0.001). Therefore, regarding patients with IMI: (1) sinus bradycardia is more frequent when the infarct-related artery is the RCA; (2) proximal occlusions of the right coronary predispose low heart rates; and (3) occlusion of the LCxA rarely induces sinus bradycardia.

Coronary artery bypass graft surgery in patients with ischemic cardiomyopathy and severe left ventricular dysfunction: short and long-term results.

BACKGROUND: We evaluated the prognostic value of preoperative parameters, surgical risk, functional benefits and long-term survival after myocardial revascularization in patients with established ischemic cardiomyopathy. METHODS: Seventy-one patients with ischemic cardiomyopathy, severe left ventricular dysfunction (left ventricular ejection fraction < 30%), and myocardial perfusion evaluated by Thallium-201 scintigraphy, were studied before and after myocardial revascularization, during hospitalization and throughout 48 months (average) of late follow-up. RESULTS: The early postoperative mortality was 2.8% and the five-year survival rate was 62.8%. When the survival rate was studied, there was no correlation with 1) the presence of Q-waves on preoperative cardiogram, 2) the presence of ischemia on Tl-201 scintigraphy, 3) the degree of left ventricular ejection fraction, or 4) the presence of angina. There was a statistically significant difference for survivors and non-survivors in the following parameters: 1) functional class IV of CHF, and 2) the presence of left bundle-branch block (LBBB). CONCLUSIONS: Our surgical results confirm that myocardial revascularization is a safe procedure, and that it increases late survival and improves the quality of life in patients with ischemic cardiomyopathy and severe left ventricular dysfunction. We also observed that due to heterogeneous coronary and myocardial patterns of ischemic cardiomyopathy, preoperative prognostic parameters are difficult to establish. Preoperative functional class IV congestive heart failure, and LBBB were the main predictors of poor outcome following surgical revascularization for ischemic cardiomyopathy.

[Gemfibrozil reduces elevated lipoprotein (a) levels in hypercholesterolemic patients]. / O gemfibrozil reduz níveis elevados de lipoproteína (a) em pacientes hipercolesterolêmicos.

PURPOSE: To compare the effects of gemfibrozil and lovastatin in patients with hypercholesterolemia and increased lipoprotein(a) [Lp(a)] levels. METHODS: Twenty-seven subjects with total cholesterol (TC) > 240 mg/dL, LDL-C > 160 mg/dL and Lp(a) > 25 mg/dL were studied. Patients were randomized to receive gemfibrozil 1200 mg/day, (n = 14, 54 +/- 7 years) or lovastatin 40-80 mg at night (n = 13, 55 +/- 9 years) for 12 weeks. Lipid profile and Lp(a) were determined at 4 and 12 weeks of treatment. RESULTS: Gemfibrozil reduced TC (-21%), LDL-C (-26%), triglycerides (TG)(-48%) and Lp(a) (-25%), increased HDL-C (+48%)(p < 0.001). Lovastatin reduced TC (-29%), LDL-C (-37%) and TG (-25%) (p < 0.001) however, it did not affect Lp(a). CONCLUSION: Besides reducing plasma LDL-C, TG and increasing HDL-C, gemfibrozil effectively lowers Lp(a) levels. Lovastatin did not affect Lp(a) levels.

Prognostic significance of ST-T segment alterations in patients with non-Q wave myocardial infarction.

OBJECTIVE: To determine whether, among patients with non-Q wave myocardial infarction, the characteristics of the segment ST-T shifts at presentation in the diagnostic electrocardiogram can identify those with more severe coronary artery disease and predict a poor clinical outcome. DESIGN: Prospective controlled clinical trial. SETTING: Primary referral medical centre. PATIENTS: 93 patients (mean (SD) 62.0 (7.5) years) were studied: 41 with non-Q wave myocardial infarction and T wave inversion and 52 with ST segment depression. Cardiac events and mortality rates were assessed over 42 months. Age, sex, risk factors, creatinine kinase MB isoenzyme peak, and left ventricular function were comparable. RESULTS: 31 patients with T wave inversion myocardial infarction (94.6%) had total occlusion of the infarct related artery, compared with 12 patients with ST segment depression myocardial infarction (26.7%) (P < 0.05). When compared with patients with T wave inversion, patients with ST segment depression had a higher incidence of cardiac events during the first month and in the 41 subsequent months: 9.6% and 30.8% v 0% (P < 0.01) and 9.8% (P < 0.02), respectively. For the same observation periods, the mortality rates in patients with T wave inversion were 4.9% and 7.3%, and in patients with ST segment depression they were 5.8% and 9.6%, respectively. CONCLUSION: These data suggest that during a non-Q wave myocardial infarction the presence of ST segment depression is related to higher rates of short and long term cardiac events when compared with T wave inversion--possibly because of a higher incidence of residual stenosis of the infarct related artery.

Beneficial effect of long-term use of a beta-blocker in patients before acute myocardial infarction.

The outcome of 38 beta-blocker users (group BB, 28 men and 10 women with a mean age of 56 +/- 4 years) was compared to that of 100 non-users (group NU, 69 men and 31 women with a mean age of 57 +/- 8 years) after acute myocardial infarction (AMI). The two groups were compared in terms of electrocardiographic (EKG) location of the AMI (anterior, inferior and lateral), EKG Q and non-Q wave infarction, clinical functional class of Forrester, serum creatine phosphokinase MB fraction (CKMB) peak release and intrahospital mortality. There were no differences between groups concerning sex or severity of coronary artery disease but arterial hypertension was 2-fold more prevalent in group BB. The EKG location of the AMI was similar in the two groups. Non-Q infarction was significantly more prevalent in group BB (37%) than in group NU (6%). The incidence of clinical functional class IV of Forrester and the serum CKMB peaks were significantly lower in group BB (2.6% vs 16.0% and 53 +/- 3 vs 68 +/- 9 IU/l, respectively). Intrahospital mortality was also significantly lower in group BB (2.6%) than in group NU (10%). These data suggest the beneficial effect of previous long-term use of beta-blockers as indicated by a lower incidence of cardiogenic shock and a significant decrease in intrahospital mortality after AMI.

Beneficial effect of long-term use of a beta-blocker in patients before acute myocardial infarction

The outcome of 38 beta-blocker users (group BB, 28 men and 10 women with a mean age of 56 ñ 4 years) was compared to that of 100 non-users (group NU, 69 men and 31 women with mean age of 57 ñ 8 years) after acute myocardial infarction (AMI). The two groups were compared in terms of electrocardiographic (EKG) location of the AMI (anterior, inferior and lateral), EKG Q and non-Q wave infarction, clincial functional class of Forrester, serum cratine phosphokinase MB fraction (CKMB) peak release and intrahospital mortality.There were no differences between groups concerning sex or severity of coronary artery disease bath arterial hypertension was 3-fold more prevalent group BB. The EKG location of the AMI was similar int he two groups. Non-Q infarction was significantly more prevalent in group BB (37 percent) than in group NU (5 percent). The incidence of clinical functional class IV of Forrester and the serum CKMB peaks were significantly lower in goup BB (2.6 percent vs 16.0 percent and 53 ñ 3 vs 68 ñ 9 UI/1, respectively. Intrahospital mortality was also significantly lower in group BB (2.6 percent) than in group NU (10 percent). These data suggest the beneficial effect of previous long-term use of beta-blockers as indicated by a lower incidence of cardiogenic shock and a significant decrease in intrahospital mortality after AMI

Effect of gemfibrozil versus lovastatin on increased serum lipoprotein(a) levels of patients with hypercholesterolemia.

The aim of this study was to determine the effect of gemfibrozil, compared with lovastatin, in patients with high levels of lipoprotein(a) and on plasma lipid profile. Twenty-seven nondiabetic patients with high levels of plasma lipids and lipoprotein(a), 19 male and eight female, aged 37-68 (mean +/- S.D. 54.2 +/- 7.5) years, were randomly assigned to 2 weeks of treatment with gemfibrozil 600 mg twice daily (14 pts.) or lovastatin 40-80 mg once daily (13 pts.). Patients had fasting plasma total cholesterol levels > or = 6.2 mmol/l, low-density lipoprotein > 4.14 mmol/l and lipoprotein(a) > 0.62 mmol/l. All patients but one had triglycerides > 2.82 mmol/l. There were no statistical differences between both groups in terms of age, sex, clinical diagnosis and previous medication. After 3 months of treatment, gemfibrozil reduced triglycerides (47.9% vs. 24.5%; P < 0.001), very low density lipoprotein (43.9% vs. 24.6%; P < 0.05), lipoprotein(a) (25.3% vs. 4.9%; P < 0.05) and increased high-density lipoprotein (34.4% vs. 11%; P < 0.01) more than lovastatin. Gemfibrozil and lovastatin reduced comparably total cholesterol (21.4% vs. 29.0%; P = NS) and low-density lipoprotein (26.5% vs. 37.3%; P = NS). The plasma levels of high-density lipoprotein and lipoprotein(a) were unchanged significantly by lovastatin. In conclusion, besides well-known efficacy in hyperlipidemia treatment, gemfibrozil also increased high-density lipoprotein and reduced lipoprotein(a), which may have important epidemiologic implications.

[Hemodynamic behavior of the right ventricle in acute inferior wall myocardial infarction: comparison between patients with and without cardiogenic shock]. / Comportamento hemodinâmico do ventrículo direito no infarto agudo de parede inferior. Comparação entre pacientes que evoleum com e sem choque.

PURPOSE: To evaluate the hemodynamic profile of patients (pts) with acute inferior wall myocardial infarction (AMI) and dysfunction of right ventricle (RV). METHODS: Ninety nine consecutive pts (aged 56.6 +/- 3.4 years), 47 men, with inferior AMI and RV dysfunction were studied. RV infarction was diagnosed based on ST segment elevation (> lmm) in precordial V4R lead and RV abnormalities found in echocardiography. All pts were undergone to bedside hemodynamic studies, by measuring mean right atrial (RAP), pulmonary artery (PAP), wedge pulmonary (PWP), and radial artery (AP) pressures and cardiac output (CO). Cardiac index (CI), pulmonary (PAR) and systemic arterial resistance (SAR) were calculated in dynes x sec x cm-5. Left ventricle (LV) ejection fraction (EF) and RV-EF were obtained by contrast ventriculography. Cardiogenic shock was diagnosed based on AP < or = 70 mmHg, RAP > or = 7 mmHg, PWP < or = 20mm Hg, CI < or = 1.8l/min/m2 and oliguria. Pts were then subdivided in 2 groups: with cardiogenic shock (group A, n = 41) with a mean age of 55.4 +/- 2.1 and without shock (group B, n = 58) with a mean age of 57.2 +/- 1.7. RESULTS: No significant differences between groups regarding RAP, PWP, AP and LVEF were observed, but compared to group B, group A had lower CI (1.3 +/- 0.3 vs 2.6 +/- 0.5 l/min/m2, p < 0.05), higher SVR (2314 +/- 252 vs 1324 +/- 324 dynes.sec.cm-5, p < 0.01), and lower RVEF (0.27 +/- 0.08 vs 0.41 +/- 0.11%, p < 0.05). CONCLUSION: Pts with inferior AMI and RV dysfunction, cardiogenic shock depends on of RV failure and is independent of a preserved LV function.

Mortality is not increased with inferior infarction associated with right ventricular infarction and atrioventricular block.

BACKGROUND: Little information is available about the relation between right ventricular infarction (RVI) and the presence of atrioventricular block. Thus, the objective of this study was to analyse a possible correlation between the conditions, which are frequently associated with inferior acute myocardial infarction (AMI). METHODS: We studied 107 patients with inferior AMI, of whom 49 had RVI, assessed by ST-segment elevation in right precordial leads (V3R-V4R) and by technetium-99m (99mTc) pyrophosphate scintigraphy. The diagnosis of atrioventricular block was made by continuous ECG monitoring during the first week of admission. RESULTS: The patients were divided into two groups: group A with RVI and group B with isolated inferior AMI. These groups were similar regarding sex, age, coronary risk factors, and time from the onset of precordial pain to hospital admission. Group A had a predominance of atrioventricular block (61.2 versus 15.5%, P < 0.0004), peak creatine kinase MB (82.5 +/- 22.4 versus 65.2 +/- 25.1 IU/l, P < 0.05), congestive heart failure or cardiogenic shock (57.1 versus 18.9%, P < 0.002), and proximal right coronary artery occlusion (80.4 versus 25.0%, P < 0.001). Non-Q-wave infarction was more frequent in group B patients (14.2 versus 34.4%, P < 0.01). The mortality rate was similar in the two groups (12.2 versus 13.7%). CONCLUSIONS: These data suggest that infarction extension from inferior wall to the right ventricle may be related to the development of atrioventricular block and does not increase mortality.