Search PubMed⌕ Search

Biomedical subjects

M T La Rovere

Publications and source records attributed to M T La Rovere.

At least 19 recordsLinked to original sources
PubMed1996

Interaction between exercise training and ejection fraction in predicting prognosis after a first myocardial infarction.

BACKGROUND: Although recent meta-analysis trials have shown that exercise training may improve survival after myocardial infarction, the mechanism of this beneficial effect is still unknown. The purpose of this study was to detect possible interactions between exercise training and predictors of prognosis after a first myocardial infarction. METHODS AND RESULTS: Patients with uneventful clinical courses after a first myocardial infarction were randomly assigned to a 4-week training period (125 patients, group 1) or to a control group (131 patients, group 2). Before randomization, all patients underwent a symptom-limited exercise test (28 +/- 2 days after myocardial infarction), 24-hour Holter monitoring, and coronary arteriography (31 +/- 3 days after the acute episode). After a mean follow-up period of 34.5 months, 18 patients had cardiac deaths (5 in group 1 and 13 in group 2). Multivariate analysis by Cox regression model showed that ejection fraction was the only independent prognostic indicator (P = .03). Evidence existed of an interaction between ejection fraction and exercise training, showing an effect of physical training on survival that depended on the patient's ejection fraction. Among patients with ejection fractions < 41%, the relative risk for an untrained patient was 8.63 times higher than for a trained patient (P = .04), whereas for ejection fractions > 40%, the estimated risks for trained and untrained patients were similar. CONCLUSIONS: These data show that exercise training may prolong survival in post-myocardial infarction patients with depressed left ventricular function. A randomized trial in such patients seems warranted.

Adult↗
PubMed1996

Linear and nonlinear dynamics of heart rate variability after acute myocardial infarction with normal and reduced left ventricular ejection fraction.

We analyzed heart rate variability (HRV) in 2 groups of patients after acute myocardial infarction with normal and reduced ejection fraction (EF) by considering both the power of the 2 major harmonic components at low and high frequency and 2 indexes of nonlinear dynamics, namely the 1/f slope and the correlation dimension D2. HRV of patients with a reduced EF was characterized by a diminished RR variance as well as a different distribution of the residual power in all frequency ranges, with lower values of the low-frequency component expressed in both absolute and normalized units, and of the low- to high-frequency ratio. In these patients we also observed a steeper slope of the negative regression line between power and frequency in the very low frequency range. The presence of a smaller fractal dimension was suggested by a lower D2. Thus, in patients after acute myocardial infarction with a reduced EF, the reduction in HRV is associated with a different distribution of the residual power in the entire frequency range, which suggests a diminished responsiveness of sinus node to neural modulatory inputs.

Case-Control Studies↗
PubMed1996

Patency of infarct-related artery. Effect of restoration of anterograde flow on vagal reflexes. ATRAMI (Automatic Tone and Reflexes After Myocardial Infarction) Investigators.

BACKGROUND: In post-myocardial infarction (MI) patients, the restoration of anterograde flow in the infarct-related artery (IRA) significantly improves survival. Limitation of infarct size and increased electrical stability of the myocardium are likely operating mechanisms for this beneficial effect. We tested the hypothesis that patency of the IRA may enhance vagal reflexes, a factor known to affect electrical stability of the infarcted myocardium. METHODS AND RESULTS: Analysis of angiographic data was performed in 359 of 1284 post-MI patients enrolled in a multicenter prospective study within 8 weeks after the index MI. All the patients underwent baroreflex sensitivity (BRS) assessment by the phenylephrine method. The BRS of the entire population averaged 8.2+/-5.5 ms/mm Hg and was significantly related to age but not to ejection fraction (EF). One-, two-, and three-vessel disease was present in 138, 96, and 99 patients, respectively, while no coronary stenosis was observed in 26. IRA patency was documented in 234 patients (65%), while in the remaining 125 (35%), the artery remained occluded. Patients with occluded IRAs had more extensive coronary disease (2 to 3 vessels, 71% versus 46%, P<.01) and more depressed left ventricular (LV) function (LVEF, 48+/-13% versus 53+/-12%, P<.001). Patency of the IRA was associated with higher BRS values (BRS, 8.9+/-5.8 versus 7.1+/-4.7 ms/mm Hg, P<.005) and with a lower incidence (9% versus 18% P<.02) of markedly depressed BRS (<3 ms/mm Hg), a condition suggested by preliminary studies to be associated with an increased risk of post-MI mortality. The association between IRA patency and BRS was more evident in anterior than in inferior MI. Multivariate regression analysis showed that age of the patient and patency of the IRA were the major independent determinants of BRS, while LVEF was weakly related to BRS and only when analyzed as a categorized variable. CONCLUSIONS: The presence of an open IRA is associated with higher baroreflex sensitivity, and this effect is largely independent of limitation of infarct size by IRA patency. These data offer new insights into the mechanisms by which coronary artery patency may affect cardiac electrical stability and survival.

Adult↗
PubMed1995

Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain?

1. It is often assumed that the power in the low- (around 0.10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects sympathetic and vagal tone [corrected] respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Boer model). 2. We have applied the De Boer model of circulatory variability to patients with varying baroreflex sensitivity to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2 Hz), which were both distinct from the controlled respiration rate (0.25 Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Boer model. The low-frequency (0.1 Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Baroreflex sensitivity.

Baroreflex sensitivity (BRS) has rapidly gained considerable attention as a result of multiple experimental and clinical reports on its prognostic value after a myocardial infarction. This article reviews the several aspects related to the use and significance of BRS. The methodology of baroreflex testing in man is described. The complex pathophysiology underlying BRS and the hypotheses proposed to explain its frequent reduction after a myocardial infarction are discussed. The section on experimental data also provides a rationale to understand the relation between increased vagal activity and reduced propensity for ventricular fibrillation. The article focuses largely on the clinical studies relating BRS and risk of cardiac mortality and also discusses the several attempts to modify this marker of reflex vagal activation.

Animals↗
PubMed1994

Effects of beta blockers (atenolol or metoprolol) on heart rate variability after acute myocardial infarction.

This study analyzed, with spectral techniques, the effects of atenolol or metoprolol on RR interval variability in 20 patients 4 weeks after the first uncomplicated myocardial infarction. Beta blocker-induced bradycardia was associated with a significant increase in the average 24-hour values of RR variance (from 13,886 +/- 1,479 to 16,728 +/- 1,891 ms2) and of the normalized power of the high-frequency component (from 22 +/- 1 to 28 +/- 2 normalized units), whereas the low-frequency component was greatly reduced (from 60 +/- 3 to 50 +/- 3 normalized units). When considering day and nighttime separately, the effects of both drugs were more pronounced in the daytime. In addition, a marked attenuation was observed in the circadian variation of the low-frequency component after beta blockade. As a result, the early morning increase of the spectral index of sympathetic modulation was no longer detectable. These results indicate that beta-blocker administration has important effects on RR interval variability and on its spectral components. The observed reduction in signs of sympathetic activation and the increase in vagal tone after beta blockade help to explain the beneficial effects of these drugs after myocardial infarction. However, the potential clinical relevance of the increase in RR variance remains to be established.

Atenolol↗
PubMed1994

Can power spectral analysis of heart rate variability identify a high risk subgroup of congestive heart failure patients with excessive sympathetic activation? A pilot study before and after heart transplantation.

BACKGROUND AND OBJECTIVES: Autonomic dysfunction seems to be involved in the progression and prognosis of severe congestive heart failure. Parasympathetic activity can still be abnormal 4-8 weeks after haemodynamic improvement by heart transplantation. To identify patients in heart failure with a more pronounced neural derangement and to analyse the changes in sympathetic and parasympathetic activity soon after heart transplantation, spectral indices of heart rate variability were assessed in 30 patients in severe heart failure and in 13 patients after heart transplantation; a group of 15 age-matched subjects served as controls. METHODS AND RESULTS: Heart rate variability was assessed by standard electrocardiography (ECG) in patients in heart failure and by oesophageal ECG in patients after heart transplantation. Compared with controls, the mean RR interval and total power were reduced in heart failure. The 30 patients showed two different patterns of heart rate variability: in 14 no power was detected in the low frequency band (0.03-0.15 Hz) (LF) and total power was mainly concentrated in the high frequency band (0.15-0.45 Hz) (HF), whereas in the remaining 16 patients power in the LF band was increased and power in HF band was reduced compared with the controls. Patients with undetectable LF had a lower mean RR interval and total power (745(25) v 864(36) ms, p < 0.05; 118(16) v 902(202) ms2, p < 0.001), higher concentration of plasma noradrenaline (635(75) v 329(54) pg/ml, p < 0.05), and worse clinical status and prognosis (4 deaths v no deaths at 6 month follow up) than patients with a dominant LF band. In the post-transplant patients both the mean PP interval of the remnant atrium and total power resembled results in the patients with heart failure; in 7 of the 13 post-transplant patients no power was detectable in the LF band: when both HF and LF power were present the results resembled those in the 16 patients in heart failure. CONCLUSIONS: These data suggest that in more advanced stages of congestive heart failure, power spectral analysis of heart rate variability allows identification of a subgroup of patients with higher sympathetic activation and poorer clinical status who are at major risk of adverse events. In the short term after cardiac transplantation the spectral profile of the rhythm variability of the remnant atrium was not improved, suggesting that parasympathetic withdrawal and sympathetic hyperactivity persist, despite the restoration of ventricular function.

Echocardiography, Transesophageal↗
PubMed1994

Scopolamine improves autonomic balance in advanced congestive heart failure.

BACKGROUND: Sympathetic hyperactivity and parasympathetic withdrawal in patients with congestive heart failure correlate closely with disease severity and overall survival. The modulating effects of drugs on the autonomic dysfunction may contribute to improve survival. Low-dose scopolamine has a vagomimetic effect in normal subjects and patients after acute myocardial infarction. We assessed whether transdermal scopolamine would increase vagal activity in patients with congestive heart failure. METHODS AND RESULTS: Heart rate variability was assessed at baseline, 24 hours after one patch of transdermal scopolamine, and 48 hours after scopolamine withdrawal in 21 patients with moderate to severe heart failure. Scopolamine increased both time- and frequency-domain parameters of heart rate variability. Specifically, the mean RR interval and its SD increased by 5.5% (P < .001) and 45% (P < .001), respectively. The change remained significant when corrected for mean heart rate with a 39% (P < .01) increase of the coefficient of variation. The absolute power of the high-frequency component was also significantly augmented. All the parameters returned to baseline after scopolamine withdrawal. Individual analysis showed that in the 7 patients in whom scopolamine did not increase mean RR interval, heart rate variability did not change. CONCLUSIONS: Transdermal scopolamine increases vagal activity as assessed by heart rate variability in patients with congestive heart failure. This autonomic modulation does not occur in all patients and can be predicted by RR interval changes. Whether such restoration of the autonomic balance might have beneficial effects in the long-term management of patients with congestive heart failure remains to be determined.

Administration, Cutaneous↗
PubMed1994

[Assessment of the autonomic nervous system after infarction and its prognostic significance].

Recently there has been increased interest in the analysis of heart rate variability (HRV) and baroreflex sensitivity (BRS) for postinfarction risk stratification. HRV and BRS are decreased in patients following myocardial infarction and both a reduced HRV and a depressed BRS identify a subgroup at higher risk of cardiac mortality and arrhythmic events. In a large trial of post-myocardial infarction patients the relative risk of mortality was 5.3 times higher in the group with depressed HRV (standard deviation of normal RR intervals over 24 hour recordings < 50 ms) than in the group with preserved HRV. These findings were later confirmed by both time domain and power spectral analysis of HRV. The predictive value of depressed HRV was found to be independent of other established risk predictors including other Holter features and left ventricular ejection fraction. By testing reflex vagal activity, in a series of 78 patients recovering from a first myocardial infarction, the risk of death increased more than 15 times in the presence of a markedly depressed BRS (< or = 3 ms/mmHg). In a subsequent study BRS was found to be the most significant predictor of induction of sustained monomorphic ventricular tachycardia at programmed electrical stimulation. BRS seems to be more valuable than HRV in the prediction of arrhythmic events by providing a relative risk four times greater than HRV to accurately predict inducibility to ventricular tachycardia. Additional data have shown that BRS but not HRV did clearly separate postinfarction patients with aborted sudden death from similar patients without ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System↗
PubMed1993

Is sympathetic neural hyperactivity in chronic heart failure affected by heart transplantation?

It has been suggested that immunosuppression with cyclosporine induces marked sympathetic neural hyperactivity in heart transplant recipients. In the present study, the resting level of sympathetic nerve activity was investigated with intraneural recording in nine patients with severe chronic heart failure (NYHA class III-IV despite ongoing therapy), in nine heart-transplanted patients with previous heart failure (NYHA class III-IV) receiving standard low-dose triple-drug immunosuppression and in six age-matched controls without cardiovascular disease. Compared to the control group, resting sympathetic nerve discharge was markedly increased in heart failure patients (92 +/- 2 vs 60 +/- 6 B/100 b, P < 0.01), sympathetic nerve activity was lower in the majority of heart failure patients after heart transplantation, and mean burst incidence was significantly lower than in the cardiac failure group (70 +/- 7, P < 0.01). The difference between transplanted patients and the control group was not statistically significant. Thus, heart transplant recipients may reduce the augmented central sympathetic drive associated with cardiac failure despite ongoing cyclosporine treatment.

Cyclosporine↗
PubMed1992

Circadian variation of spectral indices of heart rate variability after myocardial infarction.

The circadian variations of spectral indices of heart rate variability were analyzed in 20 patients 4 weeks after a first and uncomplicated myocardial infarction (MI) and in 20 control subjects. R-R interval and variance showed a characteristic day-night pattern with a significant reduction of the latter parameter in patients after MI (10,967 +/- 1109 msec2 vs 16,860 +/- 2132 msec2). Control subjects were characterized by a predominance of low-frequency (approximately 0.1 Hz) component during the day and of high-frequency (approximately 0.25 Hz) component during the night, which reflected the expected 24-hour pattern of variation of sympatho-vagal balance. A 24-hour elevation (64 +/- 3 normalized units [nu] vs 56 +/- 2 nu; p less than 0.05) of the low-frequency component and a smaller (23 +/- 2 nu vs 32 +/- 2 nu; p less than 0.05) high-frequency component during the night differentiated patients after MI from subjects. The difference between the two groups was even more evident when the 24-hour sympatho-vagal balance was assessed with the low frequency/high frequency ratio. Thus spectral analysis of heart rate variability indicates that in patients after MI there is an alteration of neural control mechanisms as indicated by the presence of signs of sympathetic activation and by the attenuation of the nocturnal increase in vagal tone.

Aged↗
PubMed1992

Autonomic nervous system adaptations to short-term exercise training.

Signs of sympathetic hyperactivity and low parasympathetic activity have been found during the acute and recovery phases of myocardial infarction and have been associated with an increased risk of cardiac mortality. Beneficial effects of physical training have been recently reported in post-myocardial infarction patients. We tested the hypothesis that physical training would be effective in improving the autonomic balance by studying 22 patients with a first and recent myocardial infarction who were randomly assigned to enter or not enter a 4-week in-hospital physical training program. Spectral indices of heart rate variability were analyzed at rest and during 70 degrees head-up tilt before and after the index training, not training period. As expected, physical training induced a significant increase in exercise duration (13.7 +/- 0.8 vs 17.1 +/- 0.1 min, p less than 0.001) and in the anaerobic threshold (9.5 +/- 0.7 vs 12.0 +/- 1.0 min, p less than 0.02) in trained patients, while no changes were observed in the untrained group. At entry, in both groups, spectral profile of heart rate variability was characterized by a predominant LF component and a smaller HF component with no further modification after head-up tilt. After 4 weeks, in resting conditions, no significant changes in spectral components were observed in both trained and untrained patients. After physical training, head-up tilt produced significant modifications in spectral profile with an increase in the LF component (84 +/- 3 vs 69 +/- 5 nu, p less than 0.01) and a decrease in the HF component (7 +/- 1 vs 19 +/- 4 nu, p less than 0.05) in trained patients, while no changes were observed in the untrained patients. Our data suggest that in postmyocardial infarction patients, 4 weeks of physical training may induce an improvement in the autonomic balance with a restoration toward normal in the reflex activity of the system.

Adaptation, Physiological↗
PubMed1992

Myocardial infarction and baroreflex sensitivity. Clinical studies.

Based on solid experimental evidence the concept has emerged that analysis of autonomic reflexes, and specifically of baroreceptive reflexes, might contribute to the identification of high risk subgroups in the post myocardial infarction phase. Accordingly, we brought this concept to clinical fruition and have performed the first clinical study to investigate the potential prognostic value of baroreflex sensitivity. The present article reviews those clinical results which indicate an almost 15 times greater risk for cardiac mortality among the patients with depressed baroreflex sensitivity. Baroreflex sensitivity has also been correlated with heart rate variability and it was found that the degree of correlation is relatively weak and such that it is not possible to predict one measure from the other. Thus, these two autonomic markers are not redundant. Among the various possibilities to induce favorable alterations in the autonomic balance, our group has selected and analyzed exercise training and the chronic administration of beta-blocking agents. Exercise training, examined in a case-control study involving 70 patients, was found to increase baroreflex sensitivity by 30%. Beta-blockers were found to augment baroreflex sensitivity in 40% of the patients tested. As a logical evolution of these studies we have initiated a large prospective collaborative study destined to enroll 1200 post myocardial infarction patients and to assess the prognostic value of baroreflex sensitivity, of heart rate variability, and of traditional markers such as left ventricular ejection fraction and late potentials.

Clinical Trials as Topic↗
PubMed1992

Autonomic nervous system and sudden cardiac death. Experimental basis and clinical observations for post-myocardial infarction risk stratification.

The analysis of the autonomic control of the heart, by means of indirect markers, may represent a new approach for identifying patients at higher risk for sudden cardiac death after a myocardial infarction. This possibility is based on the evidence that autonomic responses during acute myocardial ischemia are a major determinant of the outcome (i.e., occurrence of ventricular fibrillation or survival). Specifically, sympathetic activation can trigger malignant arrhythmias, whereas vagal activity may exert a protective effect. Several experimental observations have provided new insights on the relation between sympatho-vagal interactions and the likelihood for the occurrence of ventricular fibrillation. In an established experimental model for sudden death involving conscious dogs with a healed myocardial infarction, either depressed reflex chronotropic responses during a blood pressure rise or reduced variability of heart rate (respectively, markers of reflex and tonic cardiac vagal activity) identify dogs at greater risk to develop malignant arrhythmias during a new ischemic episode. In anesthetized cats, direct neural recording of vagal activity to the heart confirmed that vigorous reflex vagal activation during acute myocardial ischemia is associated with protection from ventricular fibrillation. Furthermore, in these experiments the reflex neural response to acute myocardial ischemia was predicted by the analysis of baroreflex sensitivity. The antifibrillatory effect of vagal activation is confirmed by the prevention of ventricular fibrillation during acute ischemia in dogs susceptible to sudden cardiac death by direct electrical stimulation of the right vagus. The clinical counterpart of these experimental data lies in three separate prospective studies showing a higher cardiac mortality in patients who after a myocardial infarction have a depressed baroreflex sensitivity or a decreased heart rate variability. A definitive answer on the role that the analysis of markers of cardiac vagal activity may play in risk stratification of patients with coronary artery disease should be provided by Autonomic Tone and Reflexes After Myocardial Infarction (ATRAMI), an ongoing prospective study. In ATRAMI, baroreflex sensitivity and heart rate variability will be assessed within 20 days after a myocardial infarction in 1,200 patients enrolled in Europe, U.S.A., and Japan with a minimum follow up of one year.

Animals↗