Effect of 1 year of lisinopril treatment on cardiac autonomic control in hypertensive patients with left ventricular hypertrophy.

In this study we evaluated in hypertensive patients the effects of drug-induced left ventricular hypertrophy regression on cardiac autonomic control, as assessed by means of heart period variability analysis. Power spectral analysis of 24-hour electrocardiographic monitoring was performed in 30 hypertensive patients with left ventricular hypertrophy at baseline, after 1 year of lisinopril treatment, and after 1 month of drug withdrawal. At the same times, patients underwent 24-hour blood pressure monitoring, echocardiographic study, and plasma renin activity assessment. Lisinopril treatment increased plasma renin activity and reduced 24-hour systolic and diastolic pressures (from 159 +/- 14 to 121 +/- 8 and from 103 +/- 7 to 80 +/- 3 mm Hg, respectively) and left ventricular mass index (from 159 +/- 33 to 134 +/- 26 g/m2); moreover, in 12 of 30 patients, left ventricular mass normalization was achieved. Drug withdrawal was followed by an increase in blood pressure without left ventricular mass modification. In the total study population, only high-frequency power was higher after lisinopril treatment. In the subgroup of patients with left ventricular mass normalization, daytime and nighttime high-frequency powers as well as nighttime total and very-low-frequency powers were higher after 1 year of treatment than at baseline. In the remaining 18 patients, power spectral measures after treatment were slightly lower than at baseline and were even lower after drug withdrawal. Thus, in hypertensive hypertrophic patients, lisinopril treatment improves sympathovagal imbalance when left ventricular mass normalization is achieved. In patients without left ventricular mass normalization, drug withdrawal is followed by a worsening of neural cardiac control.

Power spectral analysis of heart period variability in hypertensive patients with left ventricular hypertrophy.

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.

Effects of converting enzyme inhibition on heart period variability in patients with acute myocardial infarction.

BACKGROUND: Heart period variability provides useful prognostic information on autonomic cardiac control, and a strong association has been demonstrated after myocardial infarction (MI) between cardiac mortality, sudden death, and reduced total power, ultralow-frequency (ULF) power, and very-low-frequency (VLF) power. Converting enzyme inhibitors are widely used in MI patients, but their influence on heart period variability remains to be defined. METHODS AND RESULTS: Time- and frequency-domain measures of heart period variability were calculated from 24-hour Holter monitoring in 40 patients with a first uncomplicated MI. After baseline examination between 48 and 72 hours after symptom onset, patients were randomly assigned to placebo or captopril administration, and on the third day, 24-hour Holter monitoring was repeated. No changes in time and frequency domain were detectable after placebo. After captopril, the SD of all normal RR (NN) intervals (SDNN) increased from 90 +/- 29 to 105 +/- 30 milliseconds (P < .01); the SD of the average NN intervals for all 5-minute segments (SDANN index) and the mean of the SDs of all NN intervals for all 5-minute segments (SDNN index) also increased from 74 +/- 24 to 90 +/- 26 milliseconds (P < .01) and from 45 +/- 17 to 49 +/- 15 milliseconds (P < .05), respectively. The root mean square successive difference (r-MSSD) and the percent of differences between adjacent NN intervals > 50 milliseconds (pNN50) remained unchanged. In regard to frequency-domain measures, after captopril, total power (ln unit) increased from 8.28 +/- 0.42 to 8.47 +/- 0.30 (P < .01); considering the frequency bands, a significant increase was observed in ULF (P < .01), VLF (P < .05), and low-frequency (LF) power (P < .05), whereas high-frequency (HF) power remained unchanged. CONCLUSIONS: This study supports the hypothesis that the renin-angiotensin system modulates the amplitude of ULF and VLF power. Furthermore, it demonstrates that in MI patients, converting enzyme inhibition favorably modifies measures of heart period variability strongly associated with a poor prognosis.

Prognostic value of myocardial hypoperfusion indexes in patients with suspected or known coronary artery disease.

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.

Continuous electrocardiographic monitoring for more than one hour does not improve the prognostic value of ventricular arrhythmias in survivors of first acute myocardial infarction.

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 than > or = 10 VPCs/hour (p < 0.05) 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 of > 1 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.

Effects of acetylstrophanthidin on baroreflex sensitivity in patients with acute myocardial infarction.

We evaluated the effects of acetylstrophanthidin on baroreflex sensitivity in patients soon after an acute myocardial 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.(ABSTRACT TRUNCATED AT 250 WORDS)

[Cardiac changes induced by deconditioning in athletes: an echocardiographic and electrocardiographic study]. / Modificazioni cardiache indotte dal decondizionamento nell'atleta: studio ecocardiografico ed elettrocardiografico.

The relationships between echocardiographic and electrocardiographic variations and the sensibility of three different electrocardiographic criteria of left ventricular (LV) hypertrophy were assessed during deconditioning in 18 top-level oarsmen (mean age 23 +/- 4 years). After seven months of training and on the 7th and 21st deconditioning days the oarsmen underwent clinical examination, electrocardiogram (ECG) and echocardiogram with Doppler evaluation. The following ECG measurements were obtained: heart rate (HR), QTc, QRS and T waves axes, QRS and T wave angular gradients, R, S and T wave amplitude and T wave area. Moreover, the sums of S wave in lead V1 plus R wave in lead V5 or V6, of S wave in lead V1 or V2 plus R wave in lead V5 or V6, and of R wave in lead aVL plus S wave in lead V3 were calculated as indices of left ventricular hypertrophy. The following echocardiographic parameters were also analyzed: intraventricular septal (IVST) and posterior wall thickness (PWT), LV internal diameter (LVID), left ventricular mass (LVM) and volumes, LV endocardial/epicardial diastolic surface area ratio, peak systolic meridional wall stress (PSS), end-systolic stress (ESS) and mean systolic wall stress (MWSI), LV ejection fraction (EF) and total peripheral resistances (TPR); early (E) and late (A) transmitral peak flow velocity, E/A ratio. Systolic blood pressure was reduced after 3 deconditioning weeks, while diastolic blood pressure and HR were unchanged. Left ventricular mass and end-systolic volume were reduced after 1 week, while LV end-diastolic volume only after 3 weeks; therefore, EF improved at the end of the first week when TPR were lower. End-systolic stress always remained unchanged; PSS increased at 1 week and then returned to previous values. In addition, the endocardial-epicardial area ratio increased after 1 week and then returned to starting values after 3 weeks. Doppler parameters were in the normal range and remained unchanged during the study. Amplitudes of R wave in aVL, V5, V6 and of S wave in V2 did not change, while S wave amplitude in V1 and V3 decreased after three weeks and one week, respectively. The most sensible criterion for LV hypertrophy was the sum of S wave in V1 or V2 plus R wave in V5 or V6 (range from 33.3% to 22.2%); the sum of S in V1 plus R in V5 or V6 performed better than the sum of R in aVL plus S in V3.(ABSTRACT TRUNCATED AT 400 WORDS)