Search PubMed⌕ Search

Biomedical subjects

M Piepoli

Publications and source records attributed to M Piepoli.

At least 19 recordsLinked to original sources
PubMed2000

Chronic heart failure in the elderly: value of cardiopulmonary exercise testing in risk stratification.

OBJECTIVE: To assess the value of cardiopulmonary exercise testing in predicting prognosis in a cohort of elderly patients with chronic heart failure (CHF). DESIGN: A retrospective cohort study of all patients with CHF over the age of 70 years assessed between January 1992 and May 1997. SETTING: Tertiary centre. PATIENTS: 50 patients (mean (SD) age 75.9 (4.5) years, 8 women) with CHF New York Heart Association (NYHA) class I (3 patients), II (25 patients), III (20 patients), and IV (2 patients). Follow up was complete for two years in all patients. RESULTS: The patients underwent cardiopulmonary exercise testing (peak oxygen consumption 15.2 (4.5) ml/kg/min, minute ventilation/carbon dioxide production (VE/VCO(2)) slope 38.7 (11.8)); radionucleide ventriculography (left ventricular ejection fraction 32.8 (14.3)%); serum sodium measurement (139 (2.8) mmol/l); and echocardiography (left ventricular end diastolic dimension 6.1 (1.1) cm, left ventricular end systolic dimension 4.7 (1.5) cm). At the end of follow up in May 1999, 26 patients had died. The median follow up of the survivors was 47.7 months (interquartile range 31. 5-53.5 months). On univariate analysis VE/VCO(2) slope (p < 0.0001), NYHA class (p < 0.001), peak oxygen uptake (VO(2)) (p < 0.01), left ventricular end systolic dimension (p < 0.05), and serum sodium concentration (p < 0.05) had significant predictive power. Stepwise multivariate analysis identified only VE/VCO(2) slope (p < 0.01), NYHA class (p < 0.05), and peak VO(2) (p< 0.05) as conveying significant independent prognostic information. CONCLUSION: Elderly patients with CHF have a high mortality, with the majority dead within two years. Cardiopulmonary exercise testing provides important information for risk stratification within this group and its use should not be neglected.

Aged↗
PubMed2000

[Changes in the cardiac rhythm in ischemic cardiopathy].

Ventricular arrhythmia associated with ischemic heart disease has an important role in the etiology of sudden death, both in acute and chronic coronary syndromes. The etiopathogenesis of ventricular arrhythmia is strictly linked to the time-course from the occurrence of coronary occlusion. In the very acute phase of the ischemia, ventricular arrhythmias are due to a reentry mechanism, while 4-8 hours after occlusion the enhanced automatism, and triggered activity are the key mechanisms. Therefore reentry mechanisms are the main factors responsible for postinfarction arrhythmias. Also autonomic mechanisms, electrolytes and pharmacological therapy may contribute to cause arrhythmias.

Arrhythmias, Cardiac↗
PubMed2000

Very-low-frequency oscillations in heart rate and blood pressure in periodic breathing: role of the cardiovascular limb of the hypoxic chemoreflex.

In chronic heart failure, very-low-frequency (VLF) oscillations (0.01-0.04 Hz) in heart rate and blood pressure may be related to periodic breathing, although the mechanism has not been fully characterized. Groups of ten patients with chronic heart failure and ten healthy controls performed voluntary periodic breathing with computer guidance, while ventilation, oxygen saturation, non-invasive blood pressure and RR interval were measured. In air, voluntary periodic breathing induced periodic desaturation and prominent VLF oscillations when compared with free breathing in both patients [RR interval spectral power from 179 to 358 ms2 (P<0.05); systolic blood pressure (SBP) spectral power from 3.44 to 6.25 mmHg2 (P<0.05)] and controls [RR spectral power from 1040 to 2307 ms2 (P<0.05); SBP spectral power from 3.40 to 9.38 mmHg2 (P<0.05)]. The peak in RR interval occurred 16-26 s before that in SBP, an anti-baroreflex pattern. When the patients followed an identical breathing pattern in hyperoxic conditions to prevent desaturation, the VLF RR interval spectral power was 50% lower (179.0+/-51.7 ms2; P<0.01) and the VLF SBP spectral power was 44% lower (3.51+/-0.77 mmHg(2); P<0.01); similar effects were seen in controls (VLF RR power 20% lower, at 1847+/-899 ms2, P<0.05; VLF SBP power 61% lower, at 3.68+/-0.92 mmHg2, P=0.01). Low- and high-frequency spectral powers were not significantly affected. Thus periodic breathing causes oxygen-sensitive (and by implication chemoreflex-related) anti-baroreflex VLF oscillations in RR interval and blood pressure in both patients with chronic heart failure and normal controls.

Adult↗
PubMed1999

Oscillatory breathing patterns during wakefulness in patients with chronic heart failure: clinical implications and role of augmented peripheral chemosensitivity.

BACKGROUND: Oscillatory breathing patterns characterized by rises and falls in ventilation with apnea (Cheyne-Stokes respiration [CSR]) or without apnea (periodic breathing [PB]) commonly occur during the daytime in chronic heart failure (CHF). We have prospectively characterized patients with cyclical breathing in terms of clinical characteristics, indices of autonomic control, prognosis, and the role of peripheral chemosensitivity. METHODS AND RESULTS: To determine cyclical breathing pattern, power spectral analysis was applied to 30-minute recordings of respiration in 74 stable CHF patients. Analyses of heart rate variability and baroreflex sensitivity were used to assess autonomic balance. Peripheral chemosensitivity was assessed with the transient hypoxia method. We also determined whether the suppression of peripheral chemoreceptor activity (hyperoxia or dihydrocodeine) would influence the respiratory pattern. Cyclical respiration was found in 49 (66%) patients (22 [30%] CSR, 27 [36%] PB) and was associated with more advanced CHF symptoms, impaired autonomic balance, and increased chemosensitivity (0.80 and 0.75 versus 0.34 L. min(-1). %SaO(2)(-1), P<0.001, for CSR and PB versus normal breathing, respectively). Transient hyperoxia abolished oscillatory breathing in 7 of 8 patients. Dihydrocodeine administration decreased chemosensitivity by 42% (P=0.05), which correlated with improvement in respiratory pattern. Cyclical breathing predicted poor 2-year survival (relative risk 9.41, P<0.01, by Cox proportional hazards analysis), independent of peak oxygen consumption (P=0.04). CONCLUSIONS: An oscillatory breathing pattern during the daytime is a marker of impaired autonomic regulation and poor outcome. Augmented activity of peripheral chemoreceptors may be involved in the genesis of this respiratory pattern. Modulation of peripheral chemosensitivity can reduce or abolish abnormal respiratory patterns and may be an option in the management of CHF patients with oscillatory breathing.

Aged↗
PubMed1999

Impact of periodic breathing on V(O2) and V(CO2): a quantitative approach by Fourier analysis.

Oscillations in oxygen uptake (V(O2)) and carbon dioxide production (V(CO2)) in patients with chronic heart failure differ in amplitude and phase from the oscillations in ventilation (periodic breathing, PB), leading some to doubt whether they result from PB. We applied Fourier transforms to a pulmonary gas exchange model to quantify the effects of fluctuations in alveolar ventilation (V(A)). We found that PB causes oscillations in V(O2) and V(CO2), but their amplitude and phase are complex, and vary with workload. At low workloads, the relative oscillations in V(O2) and V(CO2) closely mirror the relative oscillations in V(A). But at high workloads, the metabolic oscillations are attenuated (V(O2) most severely), and the V(O2) peaks precede the ventilatory peaks significantly. This study also explains why normal controls simulating PB at higher workloads fail to reproduce the V(O2) and V(CO2) oscillations seen in spontaneous PB of heart failure.

Carbon Dioxide↗
PubMed1999

Origin of oscillatory kinetics of respiratory gas exchange in chronic heart failure.

BACKGROUND: Respiratory gas exchange measurements in patients with chronic heart failure (CHF) at rest and during exercise commonly reveal prominent slow oscillations in ventilation (V(E)), measured oxygen uptake (VO(2)), and carbon dioxide production (VCO(2)), whose origin is not clear. Voluntary simulation of periodic breathing (PB) in normals has been reported to generate a different pattern of oscillations in gas exchange from that seen in spontaneous PB. This necessitates hypothesizing that PB is caused by a primary oscillation in tissue metabolism or in cardiac output. METHODS AND RESULTS: We developed an automated method by which normal controls could be guided to breathe according to a PB pattern. The resultant metabolic oscillations closely matched those seen in spontaneous PB and had several interesting properties. At low workloads (including rest), the oscillations in VO(2) were as prominent as those in V(E) in both spontaneous PB (alpha(VO2)/alpha(VE)=0.92+/-0.04) and voluntary PB (0.93+/-0.07). However, at increased workload, the oscillations in VO(2) because less prominent than those in V(E) in spontaneous PB (intermediate workload 0.63+/-0.05, high workload 0.57+/-0.04; P<0.001) and voluntary PB (intermediate 0.66+/-0.03, high 0.48+/-0.03; P<0.001). There was no difference in the relative size of metabolic oscillations between voluntary and spontaneous PB at matched workloads (P>0.05 at low, intermediate, and high workloads). Furthermore, VO(2) peaked before V(E) in both spontaneous and voluntary PB. This time delay varied from 6.4+/-0.4 s at low ventilation, to 11.3+/-0.9 s at high ventilation (P<0.0001). CONCLUSIONS: The magnitude and phase pattern of oscillations in gas exchange of spontaneous PB can be obtained by adequately matched voluntary PB. Therefore, the gas exchange features of PB are explicable by primary ventilatory oscillation.

Adult↗
PubMed1999

Safety of oral propafenone in the conversion of recent onset atrial fibrillation to sinus rhythm: a prospective parallel placebo-controlled multicentre study.

AIM: Oral propafenone is effective in restoring sinus rhythm however the proarrhythmic effects are still unknown. The Safety Antiarrhythmic Therapy Evaluation (SATE) trial was a prospective randomized placebo-controlled multicentre study which evaluated the safety of acute oral loading dose of propafenone in patients with recent onset atrial fibrillation. Secondary end-points were to evaluate the effect of digitalis added to propafenone in ventricular rate control and the efficacy of propafenone alone or added to digitalis compared with efficacy of digitalis plus quinidine. METHODS AND RESULTS: 246 patients (126 male; 58+/-11 years) with atrial fibrillation of <48 h duration were randomly allocated to one of four groups: digitalis 0.75-1 mg i.v. plus quinidine 1100 mg (D+Q, 70 patients); propafenone 450-600 mg orally (PNF, 66 patients); propafenone 450-600 mg orally plus digitalis 0.750-1 mg i.v. (PNF+D, 70 patients); placebo (Pl, 40 patients). All patients underwent 24-h ECG Holter monitoring. Safety was assessed by evaluating the appearance of adverse events classified as mild, moderate and severe. No severe adverse events were reported. Short lasting asymptomatic atrial flutter episodes with atrio-ventricular conduction > or =2:1 were observed in 14% of the D+Q group, 21% PNF, 18% PNF+D and in 8% Pl. One patient in the D+Q group and four in the PNF+D group showed asymptomatic runs of 3-4 ventricular ectopic beats. Reversible sinus atrial blocks (<3 s) were detected in two patients of the D+Q group and in two of the PNF group. In patients with persistent atrial fibrillation the ventricular rate was similar in the four study groups. At 3 h the high efficacy of propafenone was confirmed. At the 24th hour no differences were found between active treatment and placebo arms. CONCLUSION: Propafenone in a single oral loading dose is safe and promptly effective in patients with recent onset atrial fibrillation.

Administration, Oral↗
PubMed1999

A neural link to explain the "muscle hypothesis" of exercise intolerance in chronic heart failure.

BACKGROUND: In chronic heart failure the cause of exercise limitation is still unclear: ergoreceptors, muscle afferents sensitive to exercise metabolites, are proposed as a neural link between muscular abnormalities and the limited exercise responses in this syndrome. METHODS: In 92 stable patients with heart failure (34 in New York Heart Association class I, 27 in class II, and 31 in class III) and 28 age-matched normal controls, we assessed exercise tolerance (maximal upright bicycle) and ergoreflex activity (2 dynamic hand grips: one control and one followed by 3 minutes of local circulatory occlusion to isolate the ergoreflex component by metabolite trapping). RESULTS: Patients, with respect to the controls, showed reduced exercise tolerance (peak VO2: 20 vs 33 mL/kg/min), increased ergoreflex effects on ventilation (9 vs 4 L/min), systolic pressure (37 vs 13 mm Hg), and leg vascular resistance (45 vs 22 units) (all P <.005); with the progression of the symptoms, a progressive increase in ergoreflex contribution to the ventilatory response to exercise was observed. The indexes of exercise limitation during arm and leg exercise (ie, peak VO 2, V/VCO2 slope) correlated highly with the ergoreflex contribution to ventilatory response during handgrip test ( r </= 0.7, P <.0001) but weakly with left ventricular ejection fraction (r </= 0.5). CONCLUSION: In chronic heart failure, the overactivity of the ergoreflex is related to a degree of functional limitation and appears, through direct ventilatory and cardiovascular responses, to contribute to the abnormal responses to exercise, explaining the "muscle hypothesis."

Aged↗
PubMed1999

The impact of cachexia on cardiorespiratory reflex control in chronic heart failure.

BACKGROUND: The mechanism of persistent neurohormonal and cardiorespiratory reflex abnormalities in chronic heart failure remain unclear. Also, why chronic heart failure patients who develop cachexia demonstrate a particularly abnormal neurohormonal profile and have a high risk of death is not known. Impaired reflex control within the cardiac and respiratory systems, and abnormal heart rate variability have both been linked to a poor outcome. Muscle reflexes may contribute to persistent neurohormonal overactivity in wasted patients. Thus, we hypothesized that patients with cardiac cachexia might exhibit particularly profound abnormalities in cardiorespiratory reflexes and heart ratevariability. METHODS AND RESULTS: We investigated 39 chronic heart failure patients: 13 with cardiac cachexia (non-intentional, non-oedematous, documented weight loss of >7.5% of previous normal weight over more than 6 months), and 26 non-cachectic chronic heart failure patients matched according to the severity of chronic heart failure (all men, mean age: 59 vs 60 years, NYHA functional class: 2.6 vs 2.5, peak O(2)consumption: 16.2 vs 16.8 ml. kg(-1). min(-1), left ventricular ejection fraction: 23 vs 24%, all P>0.2 for cachectic vs non-cachectic). In the assessment of the cardiorespiratory reflex control we investigated: cardiac sympathovagal balance (using spectral analysis of heart rate variability to derive low (LF, 0. 04-0.15Hz) and high frequency (HF, 0.15-0.4Hz) components), baroreflex sensitivity (using the phenylephrine method), and peripheral chemosensitivity (using the transient hypoxic method). There was a severely abnormal pattern of cardiorespiratory reflex control in patients with cachexia compared with non-cachectic patients. The former group exhibited severely impaired autonomic reflex control, characterized by an abnormal profile of heart rate variability (reduced LF component), and depressed baroreflex sensitivity (P=0.0001 and P=0.02, respectively, vs non-cachectics). Patients with cachexia also demonstrated an increased peripheral chemosensitivity (0.91 vs0.46 l. min(-1). %SaO(2)(-1), P<0.001, cachectic vs non-cachectic, respectively). In the correlation analyses the degree of impairment in the reflex control was more closely related to wasting, and to the level of neurohormonal activation (as measured by the levels of epinephrine and norepinephrine) than to conventional markers of the severity of heart failure. CONCLUSIONS: Chronic heart failure patients who developed cardiac cachexia demonstrate an abnormal reflex control within the cardiovascular and respiratory systems. The nature of the link between this phenomenon and hormonal changes and the poor prognosis of cachectic chronic heart failure patients warrants further investigation.

Cachexia↗
PubMed1999

Reproducibility of methods for assessing baroreflex sensitivity in normal controls and in patients with chronic heart failure.

Baroreflex sensitivity (BRS) conveys useful prognostic information in patients with heart disease, yet methods for its quantification suffer from poor reproducibility and test failure in some patients with heart failure. We set out to compare the short-term reproducibility and success rate of four different methods of assessing BRS in normal subjects and patients with chronic heart failure (CHF). A total of 31 patients with CHF and 18 normal controls underwent BRS testing using four techniques: (1) bolus phenylephrine (BRS(Phe)), (2) alpha-index in both low- and high-frequency bands (BRS(alphaLF) and BRS(alphaHF) respectively), (3) the sequence method (BRS(Seq)), and (4) a new 0.1 Hz controlled-breathing, time-domain analysis method (BRS(Cbr)). Each subject underwent two test episodes with each method on the same day. The average values for BRS in patients and controls respectively were: BRS(Phe), 4.4 (+/-4.4) ms/mmHg and 19.8 (+/-11.5) ms/mmHg; BRS(alphaLF), 5.6 (+/-4.1) ms/mmHg and 15.4 (+/-5.0) ms/mmHg; BRS(alphaHF), 7.1 (+/-7.0) ms/mmHg and 25.1 (+/-8.3) ms/mmHg; BRS(Seq), 7.7 (+/-6.3) ms/mmHg and 22.5 (+/-8.4) ms/mmHg; BRS(Cbr), 6.6 (+/-5.9) ms/mmHg and 22.8 (+/-10.8) ms/mmHg. The coefficients of variation (S.D. of the difference in repeated values divided by mean) in patients and controls respectively were: BRS(Phe), 85.6% and 52.2%; BRS(alphaLF), 65.9% and 33.7%; BRS(alphaHF), 99.7% and 52. 1%; BRS(Seq), 30.7% and 40.4%; BRS(Cbr), 30.7% and 19.6%. The numbers of test failures in patients were: BRS(Phen), 15; BRS(alphaLF), 7; BRS(alphaHF), 5; BRS(Seq), 14; BRS(Cbr), 1. Of the four techniques assessed for measuring BRS, the controlled breathing time-domain method yielded the best reproducibility and lowest failure rate in controls and in patients with CHF.

Adult↗
PubMed1998

Impaired baroreflex sensitivity and sympathovagal balance in syndrome X.

Alterations of autonomic nervous control of cardiac function have been described in syndrome X. The characteristics, however, of the autonomic control of the cardiovascular system in patients with syndrome X have not been adequately studied; thus, the aim of the present study was to investigate the role of baroreceptor sensitivity and sympathovagal balance in syndrome X. The study group included 12 patients with syndrome X, 12 age- and sex-matched control patients with coronary artery disease, and 12 age- and sex-matched controls with no evidence of heart disease. Baroreceptor sensitivity was evaluated by calculating the regression line relating phenylephrine-induced increases in systolic blood pressure to the attendant changes in the RR interval. Sympathovagal balance was assessed by using heart rate variability in the time and frequency domain and measuring plasma norepinephrine at rest and during incremental bicycle exercise. Baroreceptor sensitivity was significantly reduced in syndrome X compared with that in control normal subjects (7.4 +/- 1.2 vs 16.8 +/- 2.3 ms/mm Hg; p < 0.02). This was associated with a significantly lower percentage of adjacent normal RR intervals that differ by >50 ms, lower root-mean-square of the difference of adjacent RR intervals, and lower logarithmic value of the high-frequency component in patients with syndrome X compared with normal subjects. A nonsignificant trend toward lower baroreceptor sensitivity was found in patients with syndrome X compared with control ischemic patients (7.4 +/- 2 vs 12.2 +/- 1.3 ms/mm Hg). A nonsignificant trend toward a higher value of the low- to high-frequency ratio was also observed in patients with syndrome X than in both control groups. No difference was detected in norepinephrine levels either at rest or during exercise or in the exercise-induced norepinephrine increase between the 3 groups. No difference was also observed between ischemic patients and normal subjects in either baroreceptor sensitivity or heart rate variability measurements. A significant correlation (r = 0.80, p < 0.01) was found between baroreceptor sensitivity and the high-frequency component in normal controls but not for other measurements of autonomic function in the 3 groups. In conclusion, patients with syndrome X have an altered autonomic control of the cardiovascular system characterized by impaired baroreceptor sensitivity and reduced heart rate variability. Abnormal autonomic regulation of the cardiovascular system may be of pathophysiologic importance in syndrome X.

Baroreflex↗
PubMed1998

Overview and meta-analysis of randomised trials of amiodarone in chronic heart failure.

Unlike other antiarrhythmic class I drugs, amiodarone showed in preliminary studies, benefits also in patients with left ventricular dysfunction. These positive results have induced the development of large randomised controlled studies: their results are reviewed and the controversial points are discussed. In a meta-analysis of randomised controlled trials the use of amiodarone in heart failure was associated with an approximate 20 to 25% reduction in deaths. However, amiodarone was also associated with a 120 to 124% increase in side effects.

Amiodarone↗
PubMed1998

Ventilatory response to exercise correlates with impaired heart rate variability in patients with chronic congestive heart failure.

In chronic congestive heart failure (CHF) an overactivity of muscle ergoreceptors and peripheral chemoreceptors may lead to an increased ventilatory response to exercise and contribute to the autonomic imbalance. The analysis of heart rate variability (HRV), which is a reliable method of studying autonomic regulations within the cardiovascular system, showed depressed HRV indexes in CHF, but predictors of abnormal HRV pattern in CHF remain controversial. Considering a common mechanism involved in generation of both abnormal ventilation and autonomic dysfunction in CHF, we hypothesized that impaired ventilation may be better than other variables of CHF severity in determining HRV parameters. Seventy-two patients with CHF (57+/-9 years, ejection fraction: 28+/-11%) underwent cardiopulmonary exercise testing; the relation between ventilation and carbon dioxide production (VE/VCO2) was used as an index of the ventilatory response to exercise. Time and frequency-domain measurements of HRV were derived from 24-hour electrocardiographic monitoring. Patients had reduced exercise tolerance with abnormal ventilatory response (peak oxygen consumption [VO2max]: 17.8+/-5.5 ml/kg/min, VE/VCO2: 36.0+/-9.8). Correlations were found between HRV measures and etiology, New York Heart Association (NYHA) functional class, and VO2max, but the strongest relation was observed for VE/VCO2 slope (r values from -0.33 to -0.65, p <0.01). In the multiple regression analysis only VE/VCO2 was found to correlate independently with all HRV measurements. To investigate the role of peripheral chemoreceptor overactivity as the mechanism of autonomic imbalance and the increased ventilatory response to exercise, we assessed peripheral chemosensitivity in 22 patients (mean value of peripheral chemosensitivity: 0.62+/-0.34 L/min/%SaO2, significantly higher than in normal controls, mean value: 0.29+/-0.20 L/min/%SaO2 in our laboratory). The activity of the peripheral chemoreflex inversely correlated with all parameters of HRV. Increased ventilatory response to exercise correlated with depressed HRV measures in patients with CHF better than other clinical variables. An important role of the increased peripheral chemosensitivity in this relation may be relevant, being also a potential link between functional severity and sympathovagal imbalance in CHF.

Administration, Inhalation↗
PubMed1998

Effects of Class III drugs on atrial fibrillation.

The Class III antiarrhythmic drugs have been used for the treatment of atrial fibrillation (AF); however, each has specific electrophysiologic properties that delineate different safety and/or effectiveness profiles. First-generation Class III agents seem to be more effective in preventing recurrence of AF than in converting AF to sinus rhythm. The high incidence of major cardiac and noncardiac side effects in the long term often requires discontinuation of the chronic antiarrhythmic therapy. The second-generation Class III drugs, ibutilide and dofetilide, have demonstrated interesting clinical applications, especially in the setting of atrial flutter. However, their favorable antiarrhythmic effect is counterbalanced by the high incidence of severe proarrhythmias. New promising experimental data suggest that the new Ikr-ks blockers may be free from these dangerous limitations, thus extending the indication of Class III drugs in the treatment of AF.

Animals↗