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This study was designed to compare the prognostic value of predischarge ambulatory electrocardiographic monitoring for 1, 6 and 24 hours in 188 patients surviving a first acute myocardial infarction. Ventricular premature complexes (VPCs) were considered as a mean hourly rate or classified using Lown and Moss grading systems. During the 1-year follow-up 20 cardiac deaths occurred. For all 3 monitoring times, a higher number of VPCs/hour and a higher Moss grade were associated with mortality, whereas a Lown grading system gave prognostic information only for the first hour of recording. Monitoring time did not influence specificity or sensitivity in predicting mortality;or = 3 VPCs/hour showed a higher sensitivity thanor = 10 VPCs/hour (p0.05) with a comparable specificity. After 1-hour data entered the model, neither the 6- or the 24-hour data entry improved the overall likelihood ratio statistic, regardless of what VPC grading system was used. These results demonstrate that continuous electrocardiographic recordings of1 hour are unnecessary when they are to be used for detecting ventricular arrhythmia as a predictor of mortality in patients surviving a first acute myocardial infarction.

Several studies have investigated the frequency of familial dilated cardiomyopathy (FDC). However, no systematic review and meta-analysis on this topic are available. Therefore, using the PubMed, MEDLINE, Cochrane, and the ISI Web of Science databases, relevant reports published through December 2010 were identified. For the summation of prevalence findings, prevalence point estimates and 95% confidence intervals were computed using the logit transformation formula. An aggregate estimate of clinically confirmed FDC of 23% (95% confidence interval 0.17 to 0.31) was found. However, the prevalence rates reported across these studies varied widely, ranging from 2% to 65%, and the analysis showed very high heterogeneity (Q = 295, p

BACKGROUND: Baroreflex sensitivity provides useful prognostic information in patients after acute myocardial infarction. However, no data are available about the effects of converting enzyme inhibition on this variable. OBJECTIVES: The aim of the study was to evaluate the effects of angiotensin-converting enzyme inhibition on baroreflex sensitivity in patients after uncomplicated myocardial infarction. METHODS: Twenty-five patients after uncomplicated myocardial infarction underwent baroreflex sensitivity evaluation 72 to 96 h after symptom onset and after 4 days of captopril therapy. Twenty additional patients with the same characteristics were evaluated at the same time intervals before and after placebo administration to identify spontaneous baroreflex sensitivity variations. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the RR interval. RESULTS: The mean baroreflex sensitivity value increased after captopril administration from 6.5 +/- 4.2 to 11.8 +/- 6.1 ms/mm Hg (p less than 0.01) and in individual analyses increased by greater than 2 ms/mm Hg in 68% of patients. Mean plasma renin activity increased after captopril from 3.7 +/- 2.4 to 8.5 +/- 4.9 ng/ml per h (p less than 0.005). No difference was detectable in baroreflex sensitivity and plasma renin activity values according to the site of necrosis. In the control group, baroreflex sensitivity and plasma renin activity remained unchanged between the two studies. CONCLUSIONS: This study demonstrates that in patients with uncomplicated myocardial infarction, captopril significantly improves the chronotropic response to baroreceptor stimulation.

The effects of captopril and digoxin treatment on left ventricular remodeling and function after anterior myocardial infarction were evaluated in a randomized unblinded trial. Fifty-two patients with a first transmural anterior myocardial infarction and a radionuclide left ventricular ejection fraction less than 40% were randomly assigned to treatment with captopril (Group A) or digoxin (Group B). The two groups had similar baseline hemodynamic, coronary angiographic, echocardiographic and radionuclide angiographic variables. Among the 40 patients (20 in each group) who were followed up for 1 year, echocardiographic end-diastolic and end-systolic volumes were unmodified in Group A and global wall motion index was improved (p less than 0.01); in Group B, end-diastolic and end-systolic volumes increased (p less than 0.001 for both) and global wall motion index was unchanged. Rest radionuclide ejection fraction increased significantly in both groups (p less than 0.001, Group A; p less than 0.005, Group B). A comparison of the changes in the considered variables between the two groups after 1 year of treatment showed a difference in end-diastolic (p less than 0.005) end-systolic volumes (p less than 0.001) and global wall motion index (p less than 0.005) without differences in radionuclide ejection fraction, which improved to a similar degree in both groups. The results of this study suggest that captopril therapy, started 7 to 10 days after symptom onset in patients with anterior myocardial infarction and an ejection fraction less than 40%, improves both left ventricular remodeling and function and prevents left ventricular enlargement and in these patients performs better than digitalis.

To evaluate the effects of late thrombolysis on left ventricular volume and function in acute myocardial infarction, two-dimensional echocardiography and radionuclide angiography were performed before discharge and after 1 year of follow-up study in 34 patients with acute anterior myocardial infarction. Of these, 10 admitted to the coronary care unit within 4 h from the onset of symptoms were treated with recombinant tissue-type plasminogen activator (rt-PA) (Group A) and 24 admitted between 4 and 8 h after onset were randomly assigned to receive either rt-PA (Group B, n = 12) or conventional therapy (Group C, n = 12). Seven to 10 days after admission, all patients underwent cardiac catheterization and coronary angiography. Patency of the infarct-related vessel was 70% in Group A, 66% in Group B and 33% in Group C and the average Thrombolysis in Myocardial Infarction (TIMI) coronary perfusion grade was 1.9 +/- 0.8 for Group A, 1.6 +/- 1.0 for Group B and 0.84 +/- 0.95 for Group C (Group A versus Group C p less than 0.01; Group B versus Group C p less than 0.05). At predischarge evaluation, mean left ventricular end-systolic and end-diastolic volumes were higher in Group C than in Group B (p less than 0.001 and 0.05, respectively) and Group A (p less than 0.005 for both); mean left ventricular ejection fraction at rest was lower in Group C than in Group B and Group A (p less than 0.05 for both). At 1 year follow-up study, end-systolic and end-diastolic volumes remained higher in Group C than in Group B (p less than 0.05 for both) and Group A (p less than 0.005 for end-systolic volume and p less than 0.001 for end-diastolic volume); ejection fraction at rest was lower in Group C than in Groups A and B (p less than 0.05 for both); during exercise, it increased more in Group A than in Group C (p less than 0.01). Comparison of data obtained before discharge and at the 1 year follow-up study revealed a significant differences in end-systolic volume (p less than 0.05) in Group C patients and in end-diastolic volume in patients in Groups B (p less than 0.05) and C (p less than 0.001). The beneficial effect of late thrombolysis with rt-PA may be related to a reduction in myocardial expansion and thus to a favorable influence on postinfarction left ventricular remodeling.

Objective: Growth hormone (GH) resistance with a reduction of insulin-like growth factor-I (IGF-I) serum concentrations seems to be implicated in the catabolic process associated with chronic heart failure (CHF). However, data concerning the prognostic value of these alterations in CHF patients without cachexia are scant. In this study, we aimed to determine in CHF patients the prognostic value of IGF-I/GH ratio and its relationships with N-terminal brain natriuretic peptide (NT-proBNP), a known marker of prognosis in these patients. Design: We enrolled 82 non-cachectic patients, mean age 61 ± 13 years, with ejection fraction

Coronary artery disease (CAD) risk factors influence the hyperemic response in patients without coronary artery stenosis. The aim of this study was to evaluate the influence of risk factors on coronary flow reserve (CFR) estimated by 99mTc-sestamibi cardiac imaging in patients with 1-vessel CAD. Methods: Fortyeight patients with 1-vessel CAD were enrolled in the study. Systemic hypertension, hypercholesterolemia, diabetes mellitus, and cigarette smoking were considered CAD risk factors. Within 48 h, all patients underwent coronary angiography and regional CFR assessment by 99mTc-sestamibi imaging with dipyridamole (0.74 mg/kg of body weight). Eight patients had no risk factors, 14 had 1 risk factor, 18 had 2 risk factors, and 8 had 3 risk factors. Results: The mean CFR of the narrowed coronary vessel was 1.28 +/- 0.43 in the overall study population (1.52 +/- 0.30 in patients with 50%–70% stenosis and 0.94 0.75 in patients with 70% stenosis; P < 0.001). Two-factor ANOVA showed that the number of risk factors significantly affected CFR (P < 0.001) in patients with 50%–70% stenosis, whereas significance was only borderline in patients with >70% stenosis. Finally, a significant interaction among the degree of coronary artery stenosis, the number of risk factors, and the estimated CFR was found. Conclusion: CFR is inversely related to the number of conventional risk factors in patients with 1-vessel CAD and intermediate coronary artery stenosis, whereas this influence is less evident in patients with more severe stenosis.

To characterize mitral and aortic valve abnormalities we performed M-mode, two-dimensional, and pulsed Doppler echocardiography in 42 patients with active acromegaly, 22 patients cured of acromegaly, and 64 controls pair-matched with the patients for sex and age. The overall prevalence of valve abnormalities was higher in both the active patients (86% vs. 24%; P < 0.0001) and the cured patients (73% vs. 9%; P < 0.0001) than in controls. Left ventricular hypertrophy was higher in active (81% vs. 29%; P < 0.0001), but not in cured (41% vs. 14%; P = 0.09) patients than in controls. Cardiac valve abnormalities were associated with left ventricular hypertrophy in both patients and controls, without any difference between them. Conversely, among subjects without left ventricular hypertrophy, mitral and aortic abnormalities were only present in the patients (75% of active and 54% of cured), but not in controls (3% of active controls and 0% of cured controls). In conclusion, patients with active acromegaly and those cured of the disease have a high prevalence of mitral and aortic abnormalities. The persistence of valve disease in patients with cured acromegaly is likely to be correlated with the persistence of left ventricular hypertrophy, which should be carefully and continuously monitored as an aspect of the risk of cardiac dysfunction in these patients.

Gated SPECT allows combined assessment of regional myocardial perfusion and left ventricular function. The aim of this study was to address the prognostic value of gated SPECT performed during dobutamine stress testing and during rest on patients with acute myocardial infarction treated with thrombolysis. Methods: Eighty-eight consecutive patients with uncomplicated acute myocardial infarction who underwent predischarge (3-7 d after admission) dobutamine (5-40 mug/kg of body weight per minute in 3-min dose increments) and rest gated Tc-99m-sestamibi SPECT were followed for a mean of 48 mo (range, 4-64 mo). Results: Eighteen cardiac events (8 cardiac deaths and 10 nonfatal myocardial infarctions) occurred. Ischemia at dobutamine SPECT imaging (summed difference score 1) was present in 60% of the patients. In patients without ischemia, there was a lower event rate (11%), compared with patients with mild ischemia (18%) and moderate-to-severe ischemia (40%) (P < 0.05). Patients with events showed also a higher summed difference score, compared with patients without events (2.3 +/- 1.6 vs. 1.3 +/- 1.6, P < 0.05). Independent predictors of events were the number of segments with preserved 99mTc-sestamibi uptake at rest and the number of akinetic or clyskinetic segments with preserved Tc-99m-sestamibi uptake and preserved wall thickening (global chi(2) of the model, 13.6; P < 0.01). The assessment of the incremental prognostic value of variables added sequentially showed that the addition of the summed difference score added information to perfusion status at rest (P < 0.05). Combined assessment of regional myocardial perfusion and left ventricular function at rest further improved the model (P < 0.05). Conclusion: The present study indicated that predischarge Tc-99m-sestamibi gated SPECT gives prognostic information on patients recovering from acute myocardial infarction. Patients with preserved systolic wall thickening should be regarded as a high-risk subgroup, requiring closer follow-up for appropriate treatment.

OBJECTIVES: Advancing age is an independent predictor of increased mortality after acute myocardial infarction (AMI). Several hypotheses have been developed to try to explain this phenomenon, but data available about the efficacy of thrombolytic therapy in older patients are still not conclusive. The goal of this study was to investigate the efficacy of thromholysis in adult and older patients who suffered their first AMI. DESIGN: Retrospective cohort study. SETTING: A coronary care unit. PARTICIPANTS: The sample included 244 younger (aged

Patients with mild heart failure show a reduction in preload reserve mechanism during volume expansion. At this time, the effects of volume expansion on left ventricular (LV) diastolic filling in this subset of patients have not been well characterized.We evaluated the effects of acute volume loading on Doppler parameters of LV filling in 10 healthy control subjects and in 12 patients with idiopathic dilated cardiomyopathy (DCM). In patients with DCM, the effects of losartan on diastolic adaptation to volume load were also investigated.During volume loading, the healthy control subjects showed a decrease in isovolumic relaxation time (F = 5.3, P.05) but an increase in the LV peak filling rate (F = 52.9, P.001) and velocity time integral of both systolic (F = 72.8, P.001) and diastolic (F = 4.6, P.05) pulmonary venous flow. In patients with DCM, isovolumic relaxation time decreased more than in control subjects (F = 8.1, P.01), and the deceleration time of the early mitral wave was reduced (F = 26.3, P.001). Furthermore, the duration of pulmonary venous flow reversal exceeded that of mitral flow at atrial contraction (F = 28.5, P.001). After treatment with losartan, the deceleration time of early mitral wave remained unchanged, and the duration of pulmonary venous flow reversal at atrial contraction did not exceed that of mitral flow; thus, a significant treatment effect was detectable (F = 5.6, P.05; and F = 6.6, P.05, respectively).Control subjects respond to volume load with enhancement in early LV filling, whereas patients with DCM show an increase of LV filling pressure. Diastolic adaptation to volume load improves in patients with DCM after treatment with losartan.

Increased cardiovascular morbidity and mortality were reported in GH deficiency (GHD), and GH replacement can ameliorate cardiac abnormalities of adult GHD patients. To test the potential progression of untreated GHD on the cardiovascular risk and cardiac function, cardiovascular risk factors, cardiac size, and performance were prospectively evaluated in 15 GHD patients (age, 18–56 yr) who were treated with recombinant GH at the dose of 0.15–1.0 mg/d, 15 GHD patients (age, 18–56 yr) who refused GH replacement, and 30 healthy subjects (age, 18–53 yr). Electrocardiogram, systolic and diastolic blood pressure, and heart rate measurement, serum IGF-I, total cholesterol, low- and high-density lipoprotein (LDL, HDL) cholesterol, triglycerides, and fibrinogen level assay, echocardiography, and equilibrium radionuclide angiography were performed basally and after 12 months. At study entry, low IGF-I levels, unfavorable lipid profile, and inadequate cardiac and physical performance were found in GHD patients compared with controls. After 12 months of GH treatment, IGF-I levels normalized; HDL-cholesterol levels, left ventricular (LV) mass index (LVMi), left ventricular ejection fraction (LVEF) at peak exercise, peak filling rate, exercise duration and capacity significantly increased; total- and LDL-cholesterol levels significantly decreased. After 12 months in GH-untreated GHD patients, IGF-I levels remained stable, and HDL-cholesterol levels, LVEF both at rest and at peak exercise, and exercise capacity were further reduced; total- and LDL-cholesterol levels increased slightly. LVEF at rest and its response at peak exercise normalized in 60 and 53.3%, respectively, of GH-treated patients and in none of the GH-untreated patients. In conclusion, 12 months of GH replacement normalized IGF-I and improved lipid profile and cardiac performance in adult GHD patients. A similar period of GH deprivation induced a further impairment of lipid profile and cardiac performance. This finding strongly supports the need of GH replacement in adult GHD patients.

Acromegaly has relevant effects on the cardiovascular system, but few data deal with the early effects of GH and IGF-I excess. To study the early stage of acromegalic cardiomyopathy and give indirect evidence of the mechanisms underlying GH and IGF-I action on the human heart, 25 patients with uncomplicated acromegaly [15 young subjects with short-term (< or =5 yr) disease and 10 with long-term (>5 yr) disease] and 25 sex- and age- matched controls were studied. Cardiovascular risk parameters were studied by standard methods; cardiac morphology by M-mode and Doppler echocardiography, cardiac function at rest and at peak exercise by equilibrium radionuclide angiography, and vascular disease at common carotid arteries by Doppler ultrasonography. In the patient group these measurements were repeated after 6 months of treatment with octreotide- LAR (20-40 mg, im, every 28 d). Glucose, glycosylated hemoglobin, insulin, low density lipoprotein cholesterol, triglycerides, and fibrinogen levels were higher, and high density lipoprotein cholesterol levels were lower in acromegalic patients than in controls. Resting blood pressure was similar in patients and controls, whereas heart rate at rest and systolic blood pressure at peak exercise were higher in the patients. The left ventricular mass index was higher in acromegalic patients than in controls (123.3 +/- 8.9 vs. 81.5 +/- 4.3 g/m(2); P < 0.001); seven patients had left ventricular hypertrophy. Diastolic function was similar in the two groups. The ejection fraction at rest, but not at peak exercise, was significantly increased in the patients compared with controls. As a consequence the exercise-induced changes in the ejection fraction were lower in patients than controls (8.7 +/- 1.1% vs. 21.9 +/- 3.5%; P < 0.001). At common carotid ultrasonography, young patients with acromegaly had increased diastolic peak velocity and increased intima media thickness, even if neither patient nor controls had atherosclerotic plaques. Six months after OCT-LAR treatment, GH and IGF-I levels remarkably decreased in all patients; 8 (53.3%) achieved disease control. Insulin, total cholesterol, and fibrinogen levels reduced, whereas high density lipoprotein cholesterol levels increased. Both at rest and at peak exercise, heart rate significantly decreased, whereas systolic and diastolic blood pressures did not change. The left ventricular mass index was significantly reduced, but it was still higher than the control value (101.6 +/- 3.5 g/m(2); P < 0.01). The left ventricular ejection fraction at rest was significantly reduced, but its response at peak exercise was increased (16.3 +/- 2.4%), becoming similar to the control value. At common carotids, the intima media thickness of right and left arteries was significantly reduced as was the diastolic peak velocity without any change in systolic peak velocity. Short-term GH excess, despite causing enhanced cardiac performance at rest, reduces cardiac performance on effort and impairs vascular morphology. These deleterious effects of early- onset acromegaly are ameliorated by suppressing GH/IGF-I levels for 6 months.

OBJECTIVE: To characterize cardiac structure and function and cardiac autonomic control in patients with subclinical and overt hyperthyroidism. DESIGN: Thirty patients with subclinical hyperthyroidism and 30 with overt disease were selected from patients never previously treated for endocrinological disease in the outpatient clinic of our institution. Twenty normal individuals were studied as control group. METHODS: Left ventricular structure and function and cardiac autonomic control were evaluated, respectively, by two-dimensional Doppler echocardiography and by 24-h Holter recording with heart rate variability analysis. RESULTS: Patients with overt hyperthyroidism showed greater values of left ventricular end-diastolic volume (P

Patients with chronic heart failure have elevated levels of proinflammatory cytokines; however, the mechanism for their increased expression and the site of their production are unknown.Twenty-two patients with heart failure, New York Heart Association functional class II to IV, underwent hemodynamic evaluation and echocardiographic study. Blood samples for cytokine evaluation were performed in the ascending aorta, coronary sinus, inferior vena cava, and hepatic vein. Levels of tumor necrosis factor-alpha (TNF-alpha), its soluble receptors sTNF-RI and sTNF-RII, interleukin-6 (IL-6), IL-6 soluble receptor, soluble gp130, interleukin-2 soluble receptor, and soluble Fas were measured with enzyme-linked immunosorbent assay kits.IL-6 concentrations were higher in class IV patients than in class III patients, which in turn were higher than those in class II. TNF-alpha, sTNF-RI, and sTNF-RII were higher in class IV patients than in class III and II patients. Significant correlations were found between IL-6 concentrations and left ventricular end-systolic volume (r = 0.64; P.001), pulmonary wedge pressure (r = 0.56; P.01), and left ventricular ejection fraction (r = -0.56; P.01). No correlation was found between TNF-alpha and its soluble receptors and left ventricular volumes or hemodynamic measures. Finally, no difference in cytokine concentrations was found among the different sample sites.Among inflammatory cytokines, IL-6 concentrations better reflect the hemodynamic derangement in patients with heart failure. No cardiac or gut production of cytokines occurs in patients with mild to severe heart failure.

OBJECTIVE: We evaluated the effect of two calcium channel blockers, verapamil and felodipine, on heart rate variability in hypertensive patients. DESIGN: Time and frequency domain measures of heart rate variability were obtained from 24 h Holter recording in 25 previously untreated hypertensive patients without left ventricular hypertrophy, before and after 3 months of verapamil slow-release treatment (240 mg once daily) or felodipine extended-release treatment (10 mg once daily). RESULTS: Blood pressure values decreased with both drugs. Measures of heart rate variability, comparable at baseline in the two groups, were unchanged after felodipine. After verapamil, the average RR interval, the square root of the mean of the squared differences between all adjacent normal RR intervals (r-MSSD) and the percentage of differences between all adjacent normal RR intervals > 50 ms (pNN50), measures of vagal modulation of heart rate, increased (from 735 +/- 67 to 827 +/- 84 ms, P < 0.001; from 30 +/- 10 to 44 +/- 15 ms, P < 0.001; and from 3 +/- 2 to 7 +/- 6%, P < 0.01, respectively) and were higher than after felodipine. The coefficient of variation, a measure that compensates for heart rate effects, increased only after verapamil (from 5.8 +/- 1.3% to 6.6 +/- 1.0%; P < 0.05). High frequency power and its coefficient of component variance, both representing the vagal modulation of heart rate, increased after verapamil (from 5.33 +/- 0.29 to 5.80 +/- 0.27 In units, P < 0.001 and from 1.9 +/- 0.3 to 2.2 +/- 0.25%; P < 0.05). Finally, the low to high frequency power ratio, an indicator of sympathovagal balance, with a high value suggesting a sympathetic predominance, decreased after verapamil (from 2.16 +/- 0.41 to 1.36 +/- 0.35; P < 0.001), confirming the improvement in vagal modulation of heart rate. CONCLUSION: In hypertensive patients, despite a comparable anti-hypertensive effect, verapamil, but not felodipine, has favourable effect on cardiac autonomic control.

Background Decreased heart rate variability (HRV), indicating derangement in cardiac autonomic control, has been reported in patients with chronic heart failure. However, the independent and incremental prognostic value of HRV over clinical data and measures of left ventricular dysfunction has been less thoroughly investigated. This study was designed to evaluate the predictive value of HRV and Poincare plots as assessed by 24-hour Holter recording in patients with chronic heart failure. Methods Ninety-seven patients, mean age 55 ± 13 years, with radionuclide left ventricular ejection fraction ≤40% underwent echocardiographic examination and 24-hour Holter recording. Heart failure was caused by coronary artery disease in 57 patients (59%) and idiopathic dilated cardiomyopathy in 40 (41%). Results During follow-up (39 ± 18 months), 32 cardiac deaths occurred. By Cox multivariate analysis, significant predictors of death were left ventricular end-systolic volume (hazard ratio 1.04), low- to high-frequency ratio (hazard ratio 0.09), percentage of differences between successive normal R-R intervals >50 ms (hazard ratio 0.93), and age (hazard ratio 1.06). Furthermore, HRV analysis improved (P < .001) the prognostic power of a model including clinical and echocardiographic data, left ventricular ejection fraction, and ventricular arrhythmias at Holter recording, whereas the inclusion of Poincare plots did not add further predictive value. Conclusions Our investigation demonstrated that HRV has independent and incremental prognostic value in patients with chronic heart failure and seems useful to stratify patients at high risk of cardiac death. (Am Heart J 1999;138:273-84.)

PURPOSE: We aimed to evaluate in a longitudinal study the effect of intensive training on cardiac autonomic control in athletes using 24-h heart rate variability analysis. METHODS: Time and frequency domain measures of heart rate variability were calculated from 24-h Holter monitoring in 15 high level bicyclists (mean age 21 +/- 4 yr) after 1 month of detraining and after 5 months of vigorous training. At the same times echocardiographic left ventricular mass and dimensions and maximal oxygen consumption (VO2max) were assessed. RESULTS: In detrained athletes, VO2max values, left ventricular mass and dimensions, and time and frequency domain measures of vagal modulation of heart rate were higher than in a group of untrained subjects of similar age while heart rate and the low-to-high frequency ratio were lower, indicating an enhanced vagal modulation of heart rate in athletes as compared with that in control subjects. After 5 months of vigorous training, left ventricular mass and dimensions and VO2max increased in athletes, while heart rate decreased further. In contrast, no changes were detectable in time and frequency domain measures of heart rate variability over the entire 24-h and in both waking and sleeping hours. CONCLUSIONS: This study demonstrates that an increased cardiac vagal control is detectable in detrained athletes; however, after intensive training, despite a significant decrease in heart rate, time and frequency domain measures of heart rate variability reflecting cardiac vagal control remain unchanged. Thus, other mechanisms than changes in cardiac autonomic control could be involved in determining the profound bradycardia of athletes.

The role of coronary revascularization of dysfunctional myocardium with preserved thallium-201 uptake in determining the prognosis in patients after myocardial infarction remains to be defined. This study was designed to evaluate the effects of successful revascularization on survival and left ventricular (LV) function in patients with previous myocardial infarction and evidence of dysfunctional but still viable myocardium at rest-redistribution 201Tl imaging. Seventy-six consecutive patients with LV dysfunction related to previous myocardial infarction and evidence of viable myocardium at rest-redistribution 201Tl tomography were followed for 17+/-8 months. LV ejection fraction (EF) was assessed by radionuclide angiography at baseline and after 13+/-2 months. Thirty-nine patients were revascularized (group A) and 37 treated medically (group B). During the follow-up there were nine cardiac deaths. Survival rate was 97% in group A and 66% in group B (P0.01). By Cox multivariate analysis, the extent of viable myocardium was the best predictor of cardiac death (chi2=8.67, P0.01) and provided additional information to clinical and functional data (P0.01). The inclusion of revascularization as a variable improved the global chi2 of the model from 14.1 to 21.9 (P0.01). At follow-up, EF had improved by/=5% in 16 patients. By multivariate logistic analysis, the extent of viable myocardium was the best predictor of EF improvement (chi2=15.49, P0.001) and provided additional information to clinical and functional data (P0.01). The inclusion of revascularization as a variable improved the global chi2 of the model from 16.8 to 22.5 (P0.01). These results demonstrate that the total extent of dysfunctional myocardium with preserved 201Tl uptake is the strongest predictor of cardiac death in patients after myocardial infarction. Successful revascularization of dysfunctional but viable myocardium improves survival and LVEF in such patients.

This study evaluated the incremental prognostic value of 201TI reinjection imaging over clinical, exercise and thallium stress-redistribution data in patients with previous myocardial infarction and left ventricular dysfunction. METHODS: Thallium-201 reinjection after stress-redistribution SPECT was performed in 104 consecutive patients with a first Q-wave myocardial infarction (> 8 wk) and left ventricular ejection fraction < or = 40%. Follow-up data (mean 22 mo) were available for 98 patients; 16 patients underwent early revascularization procedures within 3 mo after exercise testing and were not considered for the analysis. RESULTS: During follow-up there were 13 hard events (cardiac death and myocardial infarction) and 11 soft events (coronary revascularization procedures > 3 mo after thallium imaging). With multivariate Cox regression analysis, the sum of defects at stress-redistribution imaging that were reversible or moderate irreversible after reinjection was a powerful predictor of subsequent events. The addition of thallium reinjection imaging data significantly improved the prognostic power of clinical, exercise and stress-redistribution data for the occurrence of hard events (p < 0.01). CONCLUSION: In patients with previous myocardial infarction and left ventricular dysfunction, thallium reinjection imaging provides incremental prognostic information over those obtained from conventional stress-redistribution imaging.

Autonomic dysfunction has been reported in patients with hypertrophic cardiomyopathy. To evaluate the influence of different clinical and echocardiographic features of the disease on sympathovagal balance, as assessed by heart rate variability, 33 patients with hypertrophic cardiomyopathy and 33 healthy volunteers underwent echocardiographic examination and 24-hour electrocardiogram Holter recording. Measures of vagal modulation of heart rate were lower in patients with hypertrophic cardiomyopathy than in controls, particularly in those exhibiting syncope, exertional chest pain, dyspnea, or moderate or severe mitral regurgitation. Furthermore, the age-corrected multiple regression analysis showed that the parasympathetic cardiac control was inversely related to left atrial dimension and directly related to left ventricular end-systolic dimension. Therefore in hypertrophic cardiomyopathy the parasympathetic withdrawal is more evident in patients with symptoms than in those without; the reduction in left ventricular end-systolic dimension and the increase in left atrial size are the echocardiographic features that most influence the sympathovagal balance.

Objective: This double-blind, placebo-controled randomized study was designed to compare the antihypertensive effect and tolerability of extended-release felodipine and slow-release nifedipine retard in elderly hypertensive patients. Methods: Thirty patients of both sexes (mean age 71 years) with mild to moderate essential hypertension were recruited from our hypertension outpatient clinic. After a 2-week placebo period, felodipine extended-release (felodipine ER), 10 mg once daily, nifedipine slow-release retard (nifedipine SR), 20 mg twice daily or placebo were administered to each patient for 2 weeks according to a 3 × 3 latin-square design. At the end of each treatment period, the patients underwent 24-h noninvasive blood pressure monitoring. Results: All of the patients completed the trial and no serious adverse experience was reported. In comparison with placebo, felodipine and nifedipine decreased mean 24-h diastolic blood pressure by 6.7 and 4.3 mmHg, respectively, with no significant difference between the two drugs. Mean 24-h systolic blood pressure also decreased after felodipine and nifedipine, with no difference between the two drugs. Both drugs reduced blood pressure variability, lowering the 24-h mean standard deviation of mean hourly blood pressure values. The trough:peak ratio for felodipine was 80% for systolic and 75% for diastolic blood pressure. Conclusion: Felodipine ER once daily lowers blood pressure in elderly hypertensives and is as effective as nifedipine SR twice daily. The high trough:peak ratio suggests that the dose and the between-dose interval of felodipine provides adequate therapeutic coverage.

BACKGROUND: We evaluated the independent and incremental prognostic value of cardiac catheterization and coronary angiographic data over thallium reinjection after stress redistribution imaging in patients with myocardial infarction and left ventricular dysfunction. METHODS AND RESULTS: Sixty-nine patients with a first myocardial infarction (> 8 weeks) and left ventricular ejection fraction < or = 40% underwent thallium-201 reinjection after stress redistribution tomographic imaging and cardiac catheterization. During follow-up (mean 26 months) 11 cardiac events (8 cardiac deaths and 3 nonfatal myocardial infarctions) occurred. On Cox regression analysis independent predictors of cardiac events were the sum of reversible and moderately irreversible defects at thallium reinjection (chi 2, 16.4, p < 0.005) and the number of reversible defects at stress redistribution (chi 2, 5.1, p < 0.05). Moreover, thallium reinjection imaging improved the prognostic power of clinical, exercise, and stress redistribution data (p < 0.01). The inclusion of left ventricular ejection fraction produced a borderline improvement (p = 0.06), whereas the number of vessels with coronary disease did not. In contrast, in patients at high risk such as those with at least 25% of viable myocardium at reinjection, the number of diseased vessels provided additional prognostic information (p < 0.05). CONCLUSIONS: In patients with chronic ischemic left ventricular dysfunction, left ventricular ejection fraction, but not the number of diseased vessels, provides additional prognostic information to thallium imaging. Therefore coronary angiography seems unnecessary in these patients, unless a significative amount of viable myocardium is detectable.

A depressed heart rate variability (HRV) is a powerful predictor of poor outcome in myocardial infarction patients. The beneficial effect of specific interventions on its recovery has been reported, but data concerning calcium antagonists are scarce. We evaluated the effect of a phenylalkylamine derivative, verapamil, and a dihydropyridine derivative, felodipine, on time-and frequency-domain measurements of HRV by 24-hour Holter monitoring in 60 patients with acute myocardial infarction (AMI). After a first Holter recording (65 ± 8 hours from the onset of symptoms), patients were randomly assigned to continue standard treatment or to also receive verapamil retard (120 mg 3 times daily) or felodipine extended-release (10 mg/day). Holter recording was repeated after 7 days. After verapamil, mean RR interval increased from 823 ± 92 to 907 ± 95 ms and the SD of all normal RR (NN) intervals (SDNN) from 99 ± 24 to 120 ± 30 ms (p 50 ms (pNN50) also increased (p Heart rate variability was evaluated by means of 24-hour Holter monitoring in 60 patients with myocardial infarction, randomly assigned to standard treatment or to verapamil retard (120 mg 3 times daily) or felodipine extended-release (10 mg/day) administration. After 7 days of verapamil treatment all measures of heart rate variability significantly increased while the increase was detectable only in few components after felodipine; moreover, the low- to high-frequency ratio decreased after verapamil and remained unchanged after felodipine, suggesting that verapamil, but not felodipine, improves sympathovagal balance early after myocardial infarction.

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This study aimed to characterize sympathovagal balance by heart period power spectrum analysis in hypertensive patients with echocardiographic evidence of left ventricular hypertrophy. Twenty ambulatory patients (11 men and 9 women), aged 50 +/- 10 years, with established essential hypertension and echocardiographic left ventricular hypertrophy, performed 24-h blood pressure monitoring and electrocardiogram Holter recording on 2 consecutive days. Twenty age- and sex-matched normal subjects comprised the control group. Power spectrum analysis, performed using the fast Fourier transform algorithm, demonstrated lower values of low and high frequency power in hypertensives than in controls, while ultralow and very low frequency power were similar in the two groups. Very low frequency, low frequency, and high frequency power increased during the night in both groups, showing a similar circadian pattern. We found a direct correlation between daytime systolic (r = 0.51; P.05) and diastolic (r = 0.52; P.05) blood pressure and left ventricular mass index. Moreover, negative correlations were found between left ventricular mass index and low frequency (r = -0.47; P.05) and high frequency power (r = -0.47; P.05). There was a direct correlation between nighttime decrease in systolic blood pressure and nighttime increase in high frequency power (r = 0.45; P.05). As 24-h low frequency and high frequency power, obtained using the Fourier transform algorithm, both reflect the parasympathetic modulation of heart rate, our results demonstrate that hypertensive patients with left ventricular hypertrophy are characterized by a sympathovagal imbalance with a reduction of vagal tone that is more evident with increasing severity of hypertension.

For quantitative assessment of cardiac autonomic control, time and frequency domain measures of heart period variability were calculated by 24 h Holter recording in 10 young obese women with early-onset familial obesity and in 10 control subjects. Ultra low frequency and very low frequency power were lower in obese subjects than in controls (P < 0.05). High frequency power, a pure measure of vagal tone, was comparable between the two groups. However, low frequency power, which analysed over a 24 h Holter recording reflects parasympathetic more than sympathetic activity, was slightly lower in obese subjects than in controls (P = 0.06). Body mass index showed an inverse correlation with total power (r =-0.62; P < 0.05) and separately with ultra low (r = -0.59; P < 0.01), very low (r= -0.64; P < 0.005), low (r = -0.61; P < 0.005) and high frequency power (r =-0.53; P < 0.05). These results demonstrate a parasympathetic withdrawal increasing body weight. The reduction of ultra low frequency and very low frequency power, which are associated with sudden death, may help to explain the higher cardiovascular risk in obesity.

BACKGROUND: We evaluated the prognostic value of exercise 201Tl indexes of myocardial hypoperfusion in patients with suspected or known coronary artery disease. METHODS AND RESULTS: Patients were divided into two groups: group I consisted of 332 patients with diagnostic electrocardiographic stress test results and group II consisted of 144 patients with nondiagnostic (inadequate or uninterpretable) stress electrocardiograms. At the 2-year follow-up, 20 hard events (16 cardiac deaths and 4 nonfatal myocardial infarctions) and 80 soft events (coronary revascularization procedures) occurred in group I. Considering total events, thallium imaging provided significant prognostic information in addition to clinical and exercise stress test data in the total study population (p < 0.001) and in patients with previous myocardial infarction (p < 0.001); in patients without previous infarction, thallium imaging added incremental prognostic value only in those with positive electrocardiographic stress test results (p < 0.01). When only hard events were considered, thallium variables added further information only in patients with previous myocardial infarction (p < 0.05). In group II at the end of follow-up, 15 hard and 39 soft events had occurred. In these patients occurrence of total (p < 0.001), hard (p < 0.05), and soft (p < 0.001) events was higher in those with abnormal thallium scintigraphic results than in those without. Moreover, no clinical and exercise variable, except history of myocardial infarction, was significantly related to outcome, whereas both indexes of extent and severity of hypoperfusion were significant. CONCLUSIONS: The results of this study demonstrate that scintigraphic indexes of myocardial hypoperfusion obtained by qualitative planar thallium imaging give unique prognostic information in patients with nondiagnostic electrocardiographic stress test results. Thallium imaging provides incremental prognostic information even in patients with diagnostic electrocardiographic stress test results but not in the low-risk subset of patients without previous infarction who have negative electrocardiographic stress test results.

We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocadial infarction. Baroreflex control of heart rate is frequently depressed after acute myocardial infarction and few data are available as to the effects of pharmacological intervention on this parameter. The reflex chronotropic response to arterial baroreceptor stimulation was assessed in 29 patients with uncomplicated acute myocardial infarction in control conditions (72-96 h after symptom onset) and 30 min after acetylstrophanthidin administration. To check for spontaneous baroreflex sensitivity variations, 24 patients with the same characteristics were evaluated at the same time intervals before and after a 10-cc bolus of saline placebo. Baroreflex sensitivity was assessed by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in RR intervals. Mean baseline baroreflex sensitivity value for the whole study population was 7.4 ± 4.5 ms/mmHg and was unchanged, 7.0 ± 4.5 ms/mmHg, after acetylstrophanthidin (P=NS). Mean baroreflex sensitivity values were also comparable dividing patients according to the site of infarction both before and after acetylstrophanthidin. Despite the lack of difference in mean baroreflex sensitivity values between the two studies, at a post hoc analysis an inverse relation was found in the total study population between baseline baroreflex sensitivity values and their changes after acetylstrophanthidin (r = -0.62; P < 0.005). The inverse relation was also evident separately in anterior (r = -0.57; P < 0.05) and in inferior (r =-0.70; P < 0.005) myocardial infarction patients. In the control group no difference was observed between mean baroreflex sensitivity values obtained in the two studies, nor was there any relationship between baseline baroreflex sensitivity values and their changes after placebo administration. These data demonstrate that after myocardial infarction acetylstrophanthidin administration had no effect on mean baroreflex sensitivity value. However, this drug seems to improve baroreflex sensitivity when it is depressed and to worsen it when normal or nearly normal.

BACKGROUND: This study evaluates the incremental prognostic value of qualitative thallium-201 imaging and coronary angiography in patients with suspected or known coronary artery disease. METHODS: Within 1 month, 150 patients underwent diagnostic symptom-limited ECG stress test, thallium imaging, and coronary angiography. The incremental power of sequentially performed tests was evaluated by the overall likelihood ratio statistic. RESULTS: At 3-year follow-up, 16 patients had died from a cardiac cause, 12 had suffered a nonfatal myocardial infarction, and 34 had undergone revascularization procedures more than 60 days after testing. Considering hard events, thallium imaging did not improve the prognostic information provided by clinical exercise stress test data, while coronary angiography increased the predictive power of the combined, exercise stress test, and scintigraphic data (P < 0.001). Moreover, when thallium results were added to clinical, exercise, and coronary angiographic data, the predictive power was unchanged. When the analysis was repeated including the occurrence of late revascularization procedures, each test showed additional prognostic information to that obtained by the other combined tests (P < 0.001). CONCLUSIONS: This study demonstrates that in patients with a symptom-limited ECG stress test, coronary angiography adds prognostic information to combined clinical, exercise ECG, and thallium imaging data. The incremental prognostic value of qualitative thallium imaging is demonstrable only when late revascularization procedures are included as events.

Characteristics and prognostic significance of ischemic ST changes at predischarge Holter monitoring were evaluated in 270 consecutive postinfarction patients. The 64 patients with ST changes had a greater incidence of non-Q-wave myocardial infarction (p less than 0.01) and ventricular premature contractions (p less than 0.01); they were more frequently in Moss class greater than 2 (p less than 0.01) and they had a lower wall motion score (p less than 0.05). At 2-year follow-up, patients with ST changes had a higher incidence of cardiac death and reinfarction. At multivariate analysis, Killip class (p less than 0.01) and ST changes (p less than 0.05) were the most predictive variables; when multivariate analysis was repeated including an additional variable--the inability to perform a stress test--Killip class was the most significant variable (p less than 0.01), and the presence of ST changes showed only borderline statistical significance (p less than 0.1). In the subset of patients who did not perform the stress test, ST change was the most important variable (p less than 0.01), followed by Killip class (p less than 0.05). Thus, after myocardial infarction, ST changes during Holter monitoring are associated with a poor prognosis and appear useful for stratifying patients who do not perform exercise stress tests.

Twenty-four hour ambulatory blood pressure and electrocardiographic monitoring (Oxford method) was carried out in baseline conditions and after 15 days of therapy with a once a day administration of 240 mg verapamil slow-release in 11 elderly hypertensive patients. The 24 hour electrocardiographic monitoring (but not the blood pressure monitoring) was also carried out after 30 days of therapy. High-pressure liquid chromatography plasma concentrations of verapamil and its metabolite norverapamil were compared with the blood pressure and electrocardiographic responses. Systolic and diastolic blood pressure were significantly reduced after 15 days of therapy without circadian rhythm modification; mean heart rate was reduced after 15 and 30 days and the P-Q interval prolonged. Peak verapamil and norverapamil plasma concentrations were observed 8 hours after administration; at the 25th hour, the concentrations were respectively 60.9% and 68.3% of peak value (139.5 +/- 95.4 ng/ml and 126.4 +/- 60.9 ng/ml). Plasma levels of verapamil and norverapamil significantly correlated with heart-rate decrease. No correlation was observed between drug concentrations and systolic and diastolic blood pressure. A first-degree atrioventricular block was observed in 3 patients during therapy. Supraventricular premature contractions showed a decrease after 15 and 30 days of therapy. Thus, once a day administration of verapamil slow release is an effective anti-hypertensive medication in elderly hypertensive patients. Caution should be exercised in patients with P-Q interval prolongation and sinus bradycardia.

Standard deviation of the histogram of left ventricular phase distribution (SDP-LV) obtained by radionclide angiography (RNA) was studied in 75 acute myocardial infarction (AMI) patients, 37 with anterior or anteroseptal (Group A) and 38 with inferior, inferolateral or posterior necrosis (Group I). In order to evaluate sensitivity, specificity and accuracy of SDP-LV compared to ejection fraction (EF) and peak filling rate (DER), 16 controls and 29 patients with coronary artery disease with normal kinesis proved by angiogaphy were studied. Patients were also compared according to normal or abnormal EF and PFR. Sensitivity of PFR was better than those of EF and PFR (86.6% vs 38.7% and 70.6%, respectively). Specificity of SDP-LV was 89.6%, better than that of PFR (58.6%), but just less than that of EF (93.1%). The accuracy of SDP-LV turned out to be better than those of EF and PFR (87.5% vs 53.8% and 67.3%, respectively). Ejection fraction correlated with SDP-LV in the total study population (r=-0.54, P

The presence and the characteristics of left ventricular diastolic dysfunction in mild to moderate systemic hypertension were evaluated in 13 normotensive subjects (Group I), in 12 hypertensive subjects without (Group II) and 28 with (Group III) LV hypertrophy who underwent two-dimensional Doppler echocardiographic study. Among Group III patients, a subset (n = 12) with a dilated left ventricle was identified. Diastolic filling parameters were impaired in Group III patients while, in Group II, they were intermediate between Groups I and III. In all Group III patients normalized peak filling rate (nPFR) correlated directly with mean velocity of circumferential fibre shortening (mVCF) (r = 0.55; P less than 0.001) and inversely with left ventricular mass index (LVM) (r = -0.60; P less than 0.001), left ventricular end-diastolic diameter (LVIDd) (r = -0.63; P less than 0.001), LV peak systolic stress (LVWST) (r = -0.64; P less than 0.01). A separate analysis showed that these correlations were also present in patients without left ventricular dilation; in the subset with left ventricular dilation nPFR correlated only with LVWST (r = -0.73; P less than 0.01), but not with LVM, mVCF, LVIDd. Thus, left ventricular hypertrophy is one of the major determinants of diastolic dysfunction in hypertensives; other factors influence nPFR values in hypertensive patients when the left ventricle dilates.

Fenoterol, a β2-adrenergic agonist recently introduced to treat asthmatic disorders, inhibits antigen-induced histamine release from human basophil leukocytes and lung mast cells in a dose-dependent fashion. The dose-response inhibition curve is paralleled by a fenoterol-induced increase in the cAMP levels of human leukocyte preparations. The relationship between the effect of fenoterol and cAMP level is supported by the finding that the β2-adrenergic agonist only inhibits the first stage of antigen-induced histamine release and not the release caused by the Ca2+ ionophore, A23187. Propranolol, a competitive antagonist of β2-adrenergic receptor, blocks the inhibition of release and the cAMP accumulation caused by fenoterol. Finally, theophylline, a cAMP phosphodiesterase inhibitor, synergistically potentiates the inhibitory effect of fenoterol on histamine release and the accumulation of cAMP. These data suggest that fenoterol may modulate the in vivo release of the mediators of immediate hypersensitivity reactions via the activation of β2-adrenergic receptor linked to adenylate cyclase on human basophils and mast cells.

SummaryThe effectiveness of a new potent diuretic, xipamide, was evaluated in the treatment of patients with mild to moderate essential hypertension. The effects of daily doses of 40 mg xipamide were compared with those of 100 mg chlorthalidone with respect to systolic and diastolic blood pressure, using a double-blind crossover design. Patients received each drug for 6 weeks, the order of treatments being at random and the periods being separated by a ‘washout’ period of 7 days. The results showed that xipamide was as effective as chlorthalidone in controlling blood pressure, both in the upright and supine positions, and when administered after chlorthalidone produced a further reduction. No such further reduction occurred when chlorthalidone was given after xipamide. Serum electrolyte changes induced by the two diuretics were comparable. Both drugs were well tolerated and caused few side-effects.

The effects of two-week treatment periods with indenolol (I) and metoprolol (M) were examined by 24-hour mean blood pressure (BP) monitoring in control conditions and during exercise stress test in 7 patients with essential hypertension, using the Oxford method. Both drugs induced a significant reduction in mean BP and heart rate (HR) as compared to pretreatment values (mean BP: from 117 +/- 3 mmHg to 106 +/- 4 after I, p less than 0.05 and to 102 +/- 3 after M, p less than 0.01; HR: from 78 +/- 2 bpm to 66 +/- 2 after I, p less than 0.01 and to 67 +/- 2 after M, p less than 0.01). I and M induced a significant reduction in systolic and diastolic BP throughout the day and most of the night. During bicycle ergometer the basal and peak values of systolic and diastolic BP were significantly lower after both treatments as compared to the pretreatment values (both p less than 0.01). Our data suggest that I once a day possesses a substantial and consistent antihypertensive action, effective over most of the 24 hours.

Myocardial asynergies detected by two-dimensional echocardiography during intravenous administration of Dipyridamole (0.75 mg/kg) were evaluated in 54 patients referred for angiographic evaluation of chest pain. Technically adequate two-dimensional echocardiograms suitable for analysis were recorded in 42 of 54 (77.7%) patients studied. Thallium-201 myocardial perfusion scintigraphy, during dipyridamole test was performed in the same patients. Thirty of the 42 patients studied showed significant coronary narrowing at cardiac catheterization. Dipyridamole-induced wall motion abnormalities and myocardial perfusion defects were detected, respectively, in 19 (63.3%) and 21 (70%) of 30 patients with significant coronary artery disease. Wall by wall comparison of the distribution of dipyridamole-induced echocardiographic asynergy with reversible thallium-201 (/sup 201/Tl) perfusion defects demonstrated complete correlation in 42 segments examined. Three segments with perfusion defects at thallium scanning did not show asynergy during the test while two segments showing wall motion abnormalities during dipyridamole infusion did not manifest perfusion defects. Our study demonstrates that two-dimensional echocardiography during dipyridamole testing is useful in detecting patients with coronary artery disease. Furthermore, ventricular asynergies detected during the test show a high correspondence with site of myocardial perfusion defects at thallium scanning.

We investigated the clinical course of 57 patients with acute inferior myocardial infarction as regards anterior S-T segment depression. Thirty of them showed S-T segment depression greater than or equal to 0.15 mV in at least 2 precordial leads, and 27 did not exhibit such changes. Twenty-seven patients underwent post-infarction exercise stress test. Furthermore, coronary arteriographic findings and left ventricular performance were evaluated in 8 of these patients with and in 8 without anterior S-T segment depression. Patients with anterior S-T segment depression showed greater inferior S-T segment elevation on admission ECG and deeper Q wave in lead aVF in ECG tracings recorded 1 month later. Higher incidences of in-hospital angina (10/30 vs 2/27, P = 0.01) and of late development of cardiac failure (5/21 vs 0/19, P = 0.03) were found among patients with anterior S-T segment depression. They showed a higher overall coronary score (82.4 +/- 31.0 vs 32.5 +/- 28.9, P = 0.002) and left anterior descending artery score (44.1 +/- 20.7 vs 8.5 +/- 16.1, P = 0.0009) and a reduced ventricular performance, evaluated by ventriculography score (49.5 +/- 2.7 vs 51.8 +/- 2.4, P = 0.05). A higher incidence of mitral regurgitation, secondary to papillary muscle dysfunction, was also found among patients with anterior S-T segment depression (4/8 vs 0/8, P = 0.04). Furthermore, the degree of anterior S-T segment depression in each of these subjects was closely correlated with the corresponding difference from normal ventricular score (r = 0.86, P less than 0.01). Finally, no difference between the two groups of patients was found as to incidence of positive exercise stress tests.

The effect of a calcium antagonist drug, nifedipine, on dipyridamole thallium-201 images was assessed in 10 angina patients with positive dipyridamole test. Two dipyridamole thallium-201 tests were performed, the first in basal conditions, the second after administration of 20 mg nifedipine. After dipyridamole, heart rate and double product increased respectively from 68.0 +/- 8.2 to 94.7 +/- 11.5 beats/min (p less than 0.01) and from 9459.5 +/- 1800.2 to 12,770.0 +/- 1864.7 mmHg X beats/min (p less than 0.01). Dipyridamole when infused after nifedipine induced an increase in heart rate from 74.2 +/- 7.16 to 88.8 +/- 5.6 beats/min (p less than 0.01) and in double product from 9650.5 +/- 1348.0 to 11,399.0 +/- 1146 mmHg X beats/min (p less than 0.05). Systolic and diastolic blood pressures were unmodified during the two studies. Segment scores were comparable before and after nifedipine. Thus, nifedipine does not worsen thallium-201 myocardial images obtained during dipyridamole infusion, therefore, this test could provide an alternative to exercise thallium-201 in patients receiving calcium antagonist drugs.

The effect of increased cholinergic activity on reperfusion induced ventricular arrhythmias was studied in alpha chloralose anaesthetised dogs by administering neostigmine during a 25 min occlusion of the anterior left descending coronary artery. The dogs were divided into five groups, each of 10 animals: the control group received only saline solution; group 1 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion (that is, 5 min before reperfusion); group 2 atropine 0.4 mg.kg-1 iv at 10 min of coronary occlusion and neostigmine 0.03 mg.kg-1 iv at 20 min; and group 3 neostigmine 0.03 mg.kg-1 iv at 20 min of coronary occlusion and at the same time underwent atrial pacing at the same rate as that of the sinus node just before neostigmine administration. In group 4 heart rate was slowed (junctional rhythm) by destroying the sinus node at 20 min of coronary occlusion. The results obtained showed that ventricular tachycardia and fibrillation, which occur at the beginning of reperfusion, were significantly less frequent in group 1 (p less than 0.001) and in group 4 (p less than 0.001). The protective action of neostigmine was abolished by previous administration of atropine (group 2) and modified by preventing the decrease in the heart rate by atrial pacing (group 3). In group 3 ventricular tachycardia was more frequent but the incidence of ventricular fibrillation was reduced significantly compared with the control and atropine groups. Thus cholinergic activity has a protective role in reperfusion arrhythmias by decreasing the heart rate before release of the coronary occlusion and therefore reduces the incidence of ventricular fibrillation.

This study was undertaken in order to assess the K+ sparing ability of amiloride. Thirty patients with liver cirrhosis and ascites or congestive heart failure were divided into three groups and treated with amiloride (Group A), hydrochlorothiazide (Group B) and amiloride plus hydrochlorothiazide (Group C) for 15 days. In all groups there was an increased diuresis while only in group A and C there was a statistically significant rise of K+ serum levels and a slight increment of K+ urinary loss. Total body K+ evaluated by 42K increased in group A and C while decreased in group B. Our results seem to confirm that amiloride has a mild diuretic action with a powerful K+ sparing capacity; amiloride is also able to counterbalance and reverse hydrochlorthiazide induced K+ urinary loss.

Our experiment shows that acute nifedipine administration is followed in hypertensive patients by a significant reduction of BP, whatever route of administration is chosen. It is remarkable that despite the different kinetics of absorption, at 30 minutes no difference was observed. As for the mechanism of action, PVR reduction elicited by means of the Ca ++ antagonist action of nifedipine associated with CI increase suggests a selective effect on the arterial resistance vessels similar to that of hydralazine. HR and CI increased, as reported by others, as a consequence of the sudden reduction of BP and such variations are probably responsible for the slight increase of P̄pa reported. A negative inotropic effect, however, may be excluded by the relatively constant Padp values in our patients.

This study evaluated the effects of acute isotonic volume expansion on heart rate variability (HRV) in 10 patients with dilated cardiomyopathy (DCM) and in 10 age- and sex-matched normal volunteers. Echocardiographic left ventricular volumes and HRV measurements by continuous Holter recording were assessed at baseline, at 60 and 120 min during intravenous saline load (0.9% NaCl, 0.25 ml ⋅ kg−1 ⋅ min−1), and 60 min after infusion was terminated. Data analysis was performed by repeated-measures ANOVA. After volume expansion, left ventricular ejection fraction increased ( F = 9.8; P < 0.001) in normal subjects and decreased ( F = 8.7; P < 0.001) in DCM patients. During volume expansion a significant difference was also detectable between the two groups in root-mean-square successive difference ( F = 25.2; P < 0.001), percentage of differences between successive normal R-R intervals >50 ms ( F = 97.6; P < 0.001), high-frequency power ( F = 50.1; P < 0.001), and low-frequency power ( F = 41.6; P < 0.001), all of which reflect parasympathetic modulation of heart rate; in fact, these measurements increased in normal subjects and decreased in DCM patients. In normal subjects, the increase in HRV measurements during volume expansion suggests a parasympathetic activation, mediated by stimulation of cardiopulmonary and arterial mechanoreceptors. On the contrary, in DCM patients the parasympathetic withdrawal, already detectable at baseline, increases during volume expansion.

The aim of this study was to evaluate the role of 99mTc-sestamibi cardiac imaging and dobutamine echocardiography in detecting myocardial viability early after acute myocardial infarction. METHODS: Forty-nine patients (mean age 52 +/- 10 y) underwent coronary angiography, low-dose dobutamine echocardiography, radionuclide angiography and rest 99mTc-sestamibi imaging within 10 d after myocardial infarction. Of these patients, 19 were revascularized and 30 were treated medically. Resting echocardiogram and radionuclide angiography were repeated 8 mo later to evaluate segmental functional recovery and changes in left ventricular (LV) ejection fraction, respectively. RESULTS: In revascularized patients, 61 of 108 akinetic or dyskinetic segments showed functional recovery. In these patients, sensitivity in predicting segmental functional recovery was 87% for sestamibi imaging and 66% for dobutamine echocardiography (P < 0.001), whereas specificity and accuracy were comparable. Sestamibi activity (> or =55% of peak) was the strongest predictor of segmental functional recovery (P < 0.001) and of LV ejection fraction improvement > or =5% (P < 0.01) after revascularization. In medically treated patients, 60 of 149 akinetic or dyskinetic segments showed functional recovery. In these patients, the majority (94%) of segments with contractile reserve on dobutamine were viable on sestamibi imaging and 86% of them improved function at follow-up. Functional recovery was poor in segments without contractile reserve either with (38%) or without (62%) preserved sestamibi uptake. Inotropic response was the best predictor of segmental (P < 0.001) and global (P < 0.01) LV functional improvement in medically treated patients. CONCLUSION: Dobutamine echocardiography predicts spontaneous functional recovery after acute myocardial infarction. However, sestamibi imaging is useful to identify patients with dysfunctional myocardium without contractile reserve who may benefit from coronary revascularization.

BACKGROUND: Analysis of heart rate variability (HRV) is a valuable noninvasive method for quantifying autonomic cardiac control in humans and has been utilized during dipyridamole echocardiographic test to differentiate positive from negative test results. HYPOTHESIS: We aimed to evaluate, by means of HRV analysis, the influence of the angiographic severity of coronary artery disease on cardiac autonomic control during dipyridamole-induced myocardial ischemia. METHODS: We analyzed RR interval variability changes during dipyridamole-induced myocardial ischemia in 31 selected patients (mean age 54 +/- 9 years) with available coronary angiography and positive dipyridamole echocardiographic test. Spectral components of HRV were assessed by means of wavelet transform analysis for the last 5 min before the beginning of the test (baseline) and for 5 min after the onset of ischemia-related events (peak dipyridamole effect). RESULTS: Patients were divided into three groups according to the number of coronary diseased vessels (Group A, single-vessel disease; Group B, double-vessel disease; Group C, triple-vessel disease). No difference was detectable at baseline among the three groups. After dipyridamole, low-frequency power, a measure of sympathetic modulation of heart rate, increased and echocardiographic wall motion score index worsened in all groups (p < 0.001). The increase in low-frequency power was more evident in Group C patients than in the other two groups (p < 0.005). Furthermore, after dipyridamole, a direct correlation was found between low-frequency power and wall motion score index (r = 0.59; p < 0.001). CONCLUSIONS: These data suggest that HRV analysis performed during dipyridamole echocardiographic test provides useful information to assess the severity of coronary artery disease.

The incidence and prognostic significance of silent myocardial ischaemia in 165 patients who survived a first acute myocardial infarction were assessed by means of maximal exercise stress test and 24 h continuous ECG monitoring performed before discharge. During the 1 year follow-up period 10 cardiac deaths occurred; moreover seven patients suffered a fatal myocardial re-infarction and 14 developed unstable angina. Cardiac death occurred in five of 40 patients (12.5%) with ST segment depression on stress test by in only three of 117 (2.6%) without ST segment changes (P