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Biomedical subjects

M T La Rovere

Publications and source records attributed to M T La Rovere.

At least 19 recordsLinked to original sources
PubMed1997

Arterial baroreflex modulation of heart rate in chronic heart failure: clinical and hemodynamic correlates and prognostic implications.

BACKGROUND: In chronic heart failure (CHF), arterial baroreflex regulation of cardiac function is impaired, leading to a reduction in the tonic restraining influence on the sympathetic nervous system. Because baroreflex sensitivity (BRS), as assessed by the phenylephrine technique, significantly contributes to postinfarction risk stratification, the aim of the present study was to evaluate whether in CHF patients a depressed BRS is associated with a worse clinical hemodynamic status and unfavorable outcome. METHODS AND RESULTS: BRS was assessed in 282 CHF patients in sinus rhythm receiving stable medical therapy (age, 52+/-9 years; New York Heart Association [NYHA] class, 2.4+/-0.6; left ventricular ejection fraction [LVEF], 23+/-6%). The BRS of the entire population averaged 3.9+/-4.0 ms/mm Hg (mean+/-SD) and was significantly related to LVEF and hemodynamic parameters (LVEF, P<.005; cardiac index and pulmonary wedge pressure, P<.001 by regression analysis). Patients in NYHA classes III or IV and those with severe mitral regurgitation had markedly depressed vagal reflexes. The association of BRS with survival was described after its categorization in three groups: below the lowest quartile (<1.3 ms/mm Hg), between the lowest quartile and the median (1.3 to 3 ms/mm Hg), and above the median (>3 ms/mm Hg). During a mean follow-up of 15+/-12 months, 78 primary events (cardiac death, nonfatal cardiac arrest, and status 1 priority transplantation) occurred (27.6%). BRS was significantly related to outcome (log rank, 9.1; P<.01), with a relative risk of 2.7 (95% confidence interval, 1.6 to 4.7) for patients with the major derangement in BRS (<1.3 ms/mm Hg). At multivariate analysis, BRS was an independent predictor of death after adjustment for noninvasive known risk factors but not when hemodynamic indexes were also considered. In CHF patients with severe mitral regurgitation, however, BRS remained a strong prognostic marker independent of hemodynamic function. CONCLUSIONS: In moderate to severe CHF, a depressed sensitivity of vagal reflexes parallels the deterioration of clinical and hemodynamic status and is significantly associated with poor survival. Particularly in patients with severe mitral regurgitation the baroreceptor modulation of heart rate provides prognostic information of incremental value to hemodynamic parameters.

Adult↗
PubMed1997

Abnormal awake respiratory patterns are common in chronic heart failure and may prevent evaluation of autonomic tone by measures of heart rate variability.

BACKGROUND: Reduced heart rate variability, particularly in the Very-low-frequency (VLF) spectral band, has been found to be a marker for poor prognosis in patients after myocardial infarction, but the origin of the VLF oscillations is unclear. In this study, we demonstrate that the power of cardiovascular oscillations in the VLF band in awake patients with mild to severe chronic heart failure is greatly increased by the common occurrence of unrecognized irregularity of breathing, which may confound the use of heart rate variability measures as indexes of autonomic tone or prognosis. METHODS AND RESULTS: Among 110 consecutive patients referred for consideration of transplantation, 90 were in sinus rhythm, of whom 10 were excluded as unstable. The remaining 80 patients underwent recordings of ECG, beat-to-beat arterial oxygen saturation (SaO2), and respiration during both spontaneous and controlled breathing. During spontaneous awake breathing, 64% showed periodic breathing or Cheyne-Stokes respiration (CSR), which was associated with dominant power in the VLF band of all signals. This VLF power accounted for 55%, 77%, and 87% of heart rate variability, respectively, in patients with normal breathing, periodic breathing, and CSR. It was reduced by 48% and 62%, respectively, during controlled breathing in patients with periodic breathing or CSR. Controlled ventilation also improved oxygen saturation and markedly reduced its variability. CONCLUSIONS: Breathing disorders are surprisingly common in awake patients with poor left ventricular function and produce large VLF oscillations in heart rate variability. If measures of heart rate variability are used for prognostic purposes during both short-term and long-term recordings, the confounding effects of variable respiratory patterns should be excluded. Respiratory rehabilitation might help control potentially hazardous surges in sympathetic tone.

Adult↗
PubMed1997

Depressed arterial baroreflex sensitivity and not reduced heart rate variability identifies patients with chronic heart failure and nonsustained ventricular tachycardia: the effect of high ventricular filling pressure.

In chronic heart failure (CHF) the contributing role of increased sympathetic activity and hemodynamic dysfunction in the genesis of ventricular arrhythmias has not been well established. To assess the relation between severe ventricular arrhythmias, hemodynamic impairment, and autonomic nervous system derangement, 142 patients with CHF in sinus rhythm underwent 24-hour electrocardiographic recording, right-sided heart catheterization, and evaluation of sympathovagal balance by heart rate variability (HRV) and baroreflex sensitivity (BRS). Patients were grouped according to the absence (without nonsustained ventricular tachycardia [NSVT]; n = 87) or presence (with NSVT; n = 55) of NSVT. Patients with NSVT had higher pulmonary artery and capillary pressures and more pronounced signs of sympathetic activation and parasympathetic withdrawal compared with those without NSVT. However, logistic regression analysis revealed that depressed BRS but not reduced HRV was significantly associated with the presence of NSVT, at both univariate analysis and after adjustment for clinical and hemodynamic variables. Moreover, it was found that when depressed BRS was associated with high pulmonary capillary pressure, the odds ratio for having NSVT rose markedly from 3.8 to 6.5. In conclusion, this study indicates that in stable CHF the assessment of arterial baroreflex function, but not HRV analysis, allows identification of patients at high risk of NSVT. It is suggested that the effect of depressed BRS is strengthened by the simultaneous presence of increased myocardial wall stress. These data support the hypothesis of a contributory role of autonomic nervous system dysfunction as expressed by the inability to activate effective vagal reflexes and an indirect index of ventricular stretch in the genesis of life-threatening arrhythmias.

Autonomic Nervous System↗
PubMed1997

Baroreflex sensitivity as a cardiac and arrhythmia mortality risk stratifier.

The last two decades have provided clear evidence for the tight and casual relation existing between arrhythmic mortality and the autonomic nervous system, particularly with imbalances characterized by decreases in vagal and/or increases in sympathetic activity. A series of compelling experimental results has represented the driving force for the clinical evaluation of the potential prognostic value of baroreflex sensitivity (BRS), a measure that can provide information on the capability to augment vagal activity. This article reviews the methodology more commonly used to quantify the clinical evaluation of this parameter, and then focuses on the key clinical studies highlighting those performed in postmyocardial infarction patients. Among them the most informative is ATRAMI, a multicenter prospective study involving almost 1300 patients. The main conclusion is that both heart rate variability and BRS are strong and independent risk factors for post-infarction mortality, thus demonstrating the clinical usefulness of autonomic markers.

Animals↗
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↗