[The long-term effects of dual-chamber stimulation in 8 patients with hypertrophic obstructive cardiomyopathy and symptoms refractory to medical therapy]. / Effetti a lungo termine della stimolazione bicamerale in otto pazienti portatori di cardiomiopatia ipertrofica ostruttiva con sintomi refrattari a terapia medica.

BACKGROUND: The issue of DDD pacing as a therapeutic option for patients with obstructive hypertrophic cardiomyopathy is still under debate. Moreover, some authors stress the concept of the placebo effect of electrical therapy in this particular setting. METHODS: We retrospectively evaluated 8 symptomatic patients with obstructive hypertrophic cardiomyopathy despite medical therapy, who underwent DDD pacemaker implantation as an adjunctive therapeutic strategy. All patients were evaluated with a two-dimensional/Doppler echocardiogram at baseline, shortly after the beginning of DDD pacing and at follow-up. In 3 patients dobutamine stimulation was necessary to elicit the intraventricular gradient. RESULTS: At follow-up (21 +/- 19 months, range 1-54 months) the peak gradient declined from 86 +/- 27 to 34 +/- 27 mmHg (55.2%). In 4 patients the peak gradient sharply declined after pacemaker implantation with active pacing and remained stable throughout the follow-up. In 2 patients we noted a continuous reduction in the peak gradient during the follow-up, while in 2 patients it returned to baseline values after 1 year and 1 month, respectively, despite an early reduction with DDD pacing. All patients experienced symptomatic amelioration throughout the follow-up. Two patients developed angina at the end of our observation together with an increase in the peak gradient. CONCLUSIONS: We believe that DDD pacing may be considered as a practical therapeutic option for patients with obstructive hypertrophic cardiomyopathy who would otherwise be regarded as candidates for surgery.

[Long-term clinical assessment of single-lead VDD electric stimulation]. / Valutazione clinica a lungo termine dell'elettrostimolazione VDD monocatetere.

BACKGROUND: During the last decade single lead VDD pacing has been progressively affirmed as an electrotherapy of choice in patients with advanced atrioventricular block without alterations of the sinus function. It combines the benefits of P-synchronous ventricular pacing with an easy implant procedure when compared to the conventional DDD approach. The aim of this study was to evaluate the validity of such an approach in a large population of patients, all implanted in a single center. METHODS: From 1987 up to now, 317 patients, all affected by advanced atrioventricular block and without sinus node dysfunction, were implanted in our center with a single lead VDD pacemaker. During follow-up the persistence of a proper atrioventricular synchronization was assessed and evaluated. RESULTS: The mean follow-up was 3.9 +/- 2.7 years/patient (range 6-138 months). The 94.6% of implanted systems maintained the normal VDD pacing function. Permanent reprogramming in VVI mode was necessary in 17 patients (5.36%); in 12 (3.78%) because of chronic atrial fibrillation and in 5 (1.63%) for loss of atrial sensing. The percentage of atrial synchronization was optimal (> 98%) and acceptable (> 95%) in 81% and 19% of patients, respectively. Episodes of paroxysmal atrial fibrillation occurred in 3 patients. Neither inhibition by myopotentials nor occurrence of sinus node disease was observed during follow-up. These results are in accordance with those reported by previous studies, performed on a smaller population or on a multicenter basis, and are comparable with the results reported for conventional DDD pacemaker. CONCLUSIONS: Our results confirm the high reliability of the single lead VDD pacing system concerning the long-term persistence of a proper atrioventricular synchronization. Data showed above enforce our opinion that this pacing approach should be considered the treatment of choice in patients with advanced atrioventricular block and preserved sinus node function.

Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris, and in acute myocardial infarction.

Coronary angiographic findings were compared in patients who presented with acute myocardial infarction (AMI, n = 75), unstable angina pectoris (UAP, n = 36), or stable angina pectoris (SAP, n = 36) for > or = 2 years without evidence of any previous acute event and with an angiogram within 2 years of the initial symptoms. Angiograms were evaluated blindly for severity, extent (depending on the percentage of each coronary segment showing atherosclerosis), and pattern (discrete, < 3 loci of narrowings involving < 50% of any segment; diffuse, anything exceeding this). Patients in the SAP group had more narrowed arteries (2.4 +/- 0.7 vs 1.3 +/- 0.6 [p < 0.02] and 1.4 +/- 0.6 [p < 0.02]), more stenoses (6.0 +/- 3.3 vs 2.1 +/- 1.5 [p < 0.01] and 2.6 +/- 1.7 [p < 0.05]) and occlusions (1.3 +/- 1.1 vs 0.7 +/- 0.6 [p = 0.05] and 0.3 +/- 0.5 [p < 0.02]), and a greater extent index (0.9 +/- 0.5 vs 0.5 +/- 0.3 [p < 0.02] and 0.5 +/- 0.3 [p < 0.02]) than those in the AMI and UAP groups. Furthermore, a discrete pattern was less prevalent in patients with UAP than in those with SAP or AMI (3% vs 40% [p < 0.02] and 25% [p < 0.05], respectively). In conclusion, patients who present with acute coronary syndromes have less extensive atherosclerosis than those who present with chronic stable angina. Therefore, in the former group, coronary atherosclerosis appears to be more susceptible to ischemic stimuli responsible for acute coronary syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)

[Circadian rhythm of the heart rate and autonomic nervous system stimulation tests in patients with systemic lupus erythematosus]. / Ritmo circadiano della frequenza cardiaca e prove di stimolazione autonomica in pazienti con lupus eritematoso sistemico.

We studied 19 women (mean age 35 +/- 13 years) with systemic lupus erythematosus (SLE), in order to evaluate whether or not alterations in the circadian rhythm of heart rate (HR) occur in patients with pathologic responses to stimulation tests of the autonomic nervous system (ST-ANS). The duration of SLE was 5.3 +/- 5 years. None of the patients had clinical signs of cardiopathy or dysautonomy, nor were any of them taking drugs with known effects on the heart or ANS. Nine patients (47%, group A) had normal ST-ANS and 10 (53%, group B) had an abnormal response to at least 1 ST-ANS (5 to sympathetic ANS, 3 to parasympathetic and 2 to both ST-ANS). Age, duration of disease and therapy were not different between the 2 groups. All patients underwent 24-hour ambulatory ECG monitoring, and chronobiologic analysis of hourly HR was carried out by single and mean cosinor methods. A significant circadian rhythm was found both in the total sample (mesor 80 b/min, acrophase h 13:12; p less than 0.01), and, separately, in group A (mesor 82 b/min, acrophase h 13:11; p less than 0.01) and group B (mesor 78 b/min, acrophase h 13:12; p less than 0.01). No difference existed between the HR circadian rhythms of the 2 groups. Thus, our data show the possibility of ANS involvement in SLE patients without clinical signs of dysautonomy; the analysis of the HR circadian rhythm does not appear to be a sensitive method to identify early involvement of the ANS in these patients.

Reproducibility in circadian rhythm of ventricular premature complexes.

To evaluate the existence and reproducibility of a circadian rhythm of ventricular premature complexes (VPCs), 38 patients (mean age 57 +/- 17 years) with greater than or equal to VPCs/hour were studied with 24-hour electrocardiogram Holter monitoring. Nineteen patients had coronary artery disease and 19 had structurally normal hearts. A second Holter electrocardiogram was recorded in all patients from 2 to 47 days (mean 11) after the first. Chronobiologic analysis was made by single and mean cosinor methods. A significant and similar circadian rhythm of VPCs was found in the total sample both on the first (mesor 399, acrophase at 15:08, p less than 0.01) and the second day (mesor 306, acrophase at 14:47, p less than 0.05), with 2 main peaks, the first in the late morning and the second in the afternoon. However, only 18 patients (47%, group A) had a significant individual circadian rhythm of VPCs on both days, whereas 20 (53%, group B) did not have a significant rhythm in greater than or equal to 1 day. A high reproducibility of the circadian rhythm of VPCs was found in group A patients, with a difference of 2.1 +/- 1.8 hours between the acrophases of the 2 days, whereas the difference was 4.4 +/- 3.3 hours in group B patients (p less than 0.01). Among group A patients, 14 (78%) had a VPC rhythm with acrophase occurring during waking hours, whereas the acrophase of 4 (22%) occurred during the night. The reproducibility of the circadian rhythm of VPCs was not influenced by gender, presence of coronary disease, medical therapy, basal VPC number, or day-to-day variability of VPCs, although group A patients were older than group B patients (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)