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Biomedical subjects

R Lorenzoni

Publications and source records attributed to R Lorenzoni.

14 recordsLinked to original sources
PubMed1996

Activated pyrolytic carbon tip pacing leads: an alternative to steroid-eluting pacing leads?

Pyrolytic carbon technology is known for its excellent mechanical properties and electrical conductivity; it is particularly biocompatible and does not require high production costs. The Sorin S100/4 lead is a ventricular passive fixation lead with a hemispherical electrode surface area of 4 mm2; the stimulating tip is made of a graphite core coated by a thin activated pyrolytic carbon layer. We evaluated the acute and medium-term performance of the unipolar version of this lead in 65 patients. At implantation, pacing threshold (at 0.5 ms) was 0.26 +/- 0.08 V; pacing impedance (at 5 V and 0.5 ms) was 537 +/- 94 omega and R wave amplitude was 15.0 +/- 5.5 mV. No lead related complications (dislodgment, perforation, exit block, etc.) occurred in any patient; one patient presented with a wire fracture after 26 months, due to subclavian crush syndrome. Follow-up procedures were performed at 1 week, and 2-, 10-, 18-, and 30-months postimplant. Since the leads were connected to pacemakers from different manufacturers, either voltage or duration thresholds were measured. In approximately two thirds of the patients, with an output of 2.5 V, a mean duration threshold of 0.16 +/- 0.13 ms at 1 week, 0.12 +/- 0.08 ms at 2 months, 0.11 +/- 0.06 ms at 10 months, 0.09 +/- 0.06 ms at 18 months, and 0.07 +/- 0.03 ms at 30 months, was measured. In the remaining one-third of the patients, a comparable voltage threshold trend was measured. The mean pacing impedance showed a transient drop at 1 week, and then increased to a plateau of about 600 omega reached after 10 months. No sensing defect occurred in any patient. Our data show good acute and intermediate-term results of the S100/4 lead; the early rise in threshold was remarkably blunted. Activated pyrolytic carbon tip leads might therefore be considered as a possible, inexpensive alternative to steroid-eluting leads.

Aged↗
PubMed1996

Effect of alpha 1-adrenoceptor blockade on resting and hyperemic myocardial blood flow in normal humans.

In the present study we aimed to assess the effect of alpha 1-adrenoceptor blockade on resting and hyperemic myocardial blood flow in normal humans. Myocardial blood flow, at baseline and after dipyridamole, was measured with positron emission tomography and 15O-labeled water in 11 normal volunteers at control and during alpha 1-blockade with doxazosin. Baseline myocardial blood flow during alpha 1-blockade was not different from control, whereas coronary resistance was significantly lower (73.48 +/- 18.31 vs. 89.84 +/- 27.96 mmHg.min.ml-1.g-1; P < 0.05). After dipyridamole, myocardial blood flow during alpha 1-blockade was significantly higher (3.50 +/- 0.75 vs. 2.58 +/- 0.54 ml.min-1.g-1; P < 0.01) and coronary resistance lower (25.30 +/- 7.37 vs. 33.89 +/- 7.04 mmHg.min.ml-1.g-1; P < 0.01) compared with control. In conclusion, in normal humans, dipyridamole-induced increase in myocardial blood flow is limited by alpha 1-mediated coronary vasoconstriction.

Adrenergic alpha-Antagonists↗
PubMed1995

[Total atrioventricular block as the primary clinical manifestation of undiagnosed aortic dissection].

We describe the case of a 54-year-old male who was examined due to light chest pain experienced the previous day. The man was admitted to the cardiology division for the presence of a complete atrioventricular block. On admission the echocardiogram showed a large aortic regurgitation not present two years earlier. Suspecting an aortic dissection we performed a transesophageal echocardiography and a contrast computerized tomography: the two examinations were negative. The next days the patient had two episodes of acute pulmonary edema so he was transferred to the regional reference hospital where an hemodynamic unit and cardiac surgery division were available. There, he repeated a transesophageal echocardiography which was negative. The man had aortic valve replacement without angiography for his very critical condition. The surgeon identified a small aortic dissection, just above the aortic valve plane, which was responsible for valve leaflets prolapse and aortic regurgitation; the hematoma deepened towards the interatrial septum and atrioventricular junction justifying the atrioventricular block. In conclusion, a small aortic dissection can offer an atypical picture, and in this condition even very valuable diagnostic techniques may fail the diagnosis.

Aortic Dissection↗
PubMed1994

[Microcirculation and remodelling].

Acute myocardial infarction can produce alterations in the topography of the left ventricle both in the infarcted and remote areas. These changes as a whole, have been termed ventricular remodelling. Attention has been focused on myocyte alterations due to the remodelling process, but the myocardial wall also contains fibroblasts, which produce collagen and elastin fibers, and endothelial and smooth muscle cells which are the main constituents of the vascular wall. In left ventricular hypertrophy, a form of myocardial remodelling, structural changes of myocytes, cardiac interstitium as well as the coronary microcirculation have been found (vascular remodelling). In vivo, the function of coronary microcirculation can be evaluated by measuring myocardial blood flow and coronary reserve. In fact the study of coronary reserve in patients with left ventricular hypertrophy disclosed microcirculatory dysfunction which probably represents the functional counterpart of the structural changes already described. Positron emission tomography (PET) can noninvasively quantitate myocardial blood flow and coronary reserve in humans. Recently studies with PET disclosed microcirculatory alterations also in patients with coronary artery disease (CAD) in the absence of gross myocardial hypertrophy. In particular, after myocardial infarction, coronary vasodilator capacity has been shown to be impaired not only in the infarcted areas but also in the remote ones subtended by angiographically normal vessels. A blunted coronary reserve has been identified with PET also in remote regions from ischemia in patients with stable angina and single vessel CAD.

Angina Pectoris↗
PubMed1992

Coronary reserve and exercise ECG in patients with chest pain and normal coronary angiograms.

BACKGROUND: Coronary vasodilator reserve is reduced in some patients with a history of chest pain and angiographically normal coronary arteries. ECG changes suggestive of myocardial ischemia during exercise also can be demonstrated in a subset of these patients. METHODS AND RESULTS: We have investigated the correlation between coronary vasodilator reserve, assessed with 13N-labeled ammonia and positron emission tomography, and the ECG during exercise stress in 45 patients with a history of chest pain, angiographically normal coronary arteries, and a negative ergonovine test. ST segment depression on the ECG during exercise was present in 29 of 45 patients. Mean resting left ventricular blood flow was 1.04 +/- 0.22 ml.min-1.g-1; it increased to 1.32 +/- 0.47 ml.min-1.g-1 (p less than 0.01 versus baseline value) during atrial pacing and to 2.52 +/- 0.96 ml.min-1.g-1 (p less than 0.01 versus baseline value) after dipyridamole (0.56 mg/kg i.v.). No regional flow defects could be demonstrated in any patient during pacing or after dipyridamole. Myocardial flows after dipyridamole, however, did not show a normal frequency distribution (Kolmogorov-Smirnov test), and two patient populations could be identified. Twenty-nine (67%) patients had a mean left ventricular flow of 3.02 +/- 0.33 ml.min-1.g-1 after dipyridamole (range, 2.13-5.46 ml.min-1.g-1), and 14 (33%) patients had a mean flow of 1.48 +/- 0.29 ml.min-1.g-1 (range, 1.06-2.04 ml.min-1.g-1, p less than 0.01 versus the "high-flow group"). CONCLUSIONS: Approximately one third of patients in our series showed a reduced coronary vasodilator reserve. Although 12 of 14 patients in the "low-flow group" had ST segment depression during exercise stress, 16 of 29 patients in the high-flow group also had ST segment depression during exercise stress. Therefore, despite a good sensitivity (86%) in identifying patients with a blunted increment of coronary flow, the ECG response during exercise stress appears to have a rather low specificity (45%). This suggests that factors other than reduced coronary reserve and myocardial ischemia may play a role in the genesis of the ST segment depression in these patients.

Adult↗
PubMed1991

Coronary vasodilation is impaired in both hypertrophied and nonhypertrophied myocardium of patients with hypertrophic cardiomyopathy: a study with nitrogen-13 ammonia and positron emission tomography.

To assess regional coronary reserve in hypertrophic cardiomyopathy, regional myocardial blood flow was measured in 23 patients with hypertrophic cardiomyopathy and 12 control subjects by means of nitrogen-13 ammonia and dynamic positron emission tomography. In patients with hypertrophic cardiomyopathy at baseline study, regional myocardial blood flow was 1.14 +/- 0.43 ml/min per g in the hypertrophied (20 +/- 3 mm) interventricular septum and 0.90 +/- 0.35 ml/min per g (p less than 0.05 versus septal flow) in the nonhypertrophied (10 +/- 2 mm) left ventricular free wall. These were not statistically different from the corresponding values in control subjects (1.04 +/- 0.25 and 0.91 +/- 0.21 ml/min per g, respectively, p = NS). After pharmacologically induced coronary vasodilation (dipyridamole, 0.56 mg/kg intravenously over 4 min), regional myocardial blood flow in patients with hypertrophic cardiomyopathy increased significantly less than in control subjects both in the septum (1.63 +/- 0.58 versus 2.99 +/- 1.06 ml/min per g, p less than 0.001) and in the free wall (1.47 +/- 0.58 versus 2.44 +/- 0.82 ml/min per g, p less than 0.001). In addition, patients with hypertrophic cardiomyopathy who had a history of chest pain had more pronounced impairment of coronary vasodilator reserve than did those without a history of chest pain. After dipyridamole, coronary resistance in the septum decreased by 38% in patients without a history of chest pain, but decreased by only 14% in those with such a history (p less than 0.05). Coronary resistance in the free wall decreased by 45% in patients without and by 27% in those with a history of chest pain (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗
PubMed1991

Coronary hemodynamics and myocardial metabolism in patients with syndrome X: response to pacing stress.

Coronary hemodynamics, myocardial metabolism and left ventricular function at rest and after incremental atrial pacing were evaluated in 12 patients with stress-induced angina and ST segment depression, angiographically normal coronary arteries and no evidence of spasm, generally labeled as syndrome X, and in 10 normal subjects. At baseline study, great cardiac vein flow was comparable in patients and control subjects. During pacing, an equivalent rate-pressure product was reached in the two groups, but the slope of the relation between rate-pressure product and great cardiac vein flow was significantly less steep in patients than in normal subjects (0.0027 vs. 0.0054 ml/mm Hg.beat, p less than 0.001). Nevertheless, the left ventricular ejection fraction was comparable in both groups at rest (66 +/- 6% vs. 71 +/- 7%, p = NS) and during pacing (71 +/- 7% vs. 66 +/- 5%, p = NS). At baseline study, myocardial glucose extraction was more efficient in patients with syndrome X (p less than 0.05), but net myocardial exchange of pyruvate and alanine was, respectively, smaller and greater than in control subjects. Lactate was extracted to a similar extent in the two groups and in no instance was net lactate release observed during pacing or recovery. During pacing and recovery, patients with syndrome X showed net pyruvate release, unlike the control subjects in whom net pyruvate exchange was positive. In addition, patients with syndrome X continued to show net myocardial extraction of alanine during spacing and recovery, whereas normal subjects produced alanine throughout the study. Myocardial carbohydrate oxidation increased significantly during maximal pacing in normal subjects but not in patients, in whom it always remained below (p less than 0.01) the concurrent rate of myocardial uptake of carbohydrate equivalents (glucose, lactate, pyruvate, alanine). Myocardial energy expenditure was significantly lower in patients than in control subjects at maximal rate-pressure product levels (p less than 0.01). The metabolic pattern in patients with syndrome X therefore is not consistent with classic ischemia, although differences in the net exchange of circulating substrates (glucose, pyruvate, alanine) can be demonstrated. Thus, in patients with syndrome X, the symptoms, electrocardiographic signs and impairment in the increase in great cardiac vein flow during pacing coexist with preserved global and regional left ventricular function and myocardial energy efficiency.

Angina Pectoris↗
PubMed1991

[Psychological and social aspects in women with syndrome X].

A sizeable proportion (20-30%) of patients undergoing coronary arteriography for a chest pain syndrome are found to have angiographically normal coronary arteries. Some of these subjects (10-15%) have ischemic-like electrocardiographic changes during stress and no evidence of spasm of the epicardial coronary arteries (syndrome X). The vast majority of these patients are middle aged females. In the present investigation we evaluated the psychological and social characteristics of a group of patients with syndrome X (PX, n = 30). The results obtained in the PX group were compared with those in a sex and age matched group of patients with angiographically proven coronary artery disease (PI, n = 32) and with those in a group of control subjects (C, n = 29). Two original questionnaires were employed to collect the demographic and family data. The psychological data were obtained through the following 4 questionnaires: Symptom Rating Test (SRT); Symptom Questionnaire (SQ); Illness Behaviour Questionnaire (IBQ); Maudsley Personality Inventory (MPI). The results of our study indicated that in most of the patients with syndrome X the psychological and social conditions are similar and they are not compatible with a satisfactory lifestyle. In most cases both family and social difficulties are present, which impose excessive workload and distress on the patients. Very often the beginning of the chest pain history tends to coincide with the periods of greatest stress and with the occurrence of dramatic events in the family. On the other hand, the onset of symptoms often has the effect of releasing some of the environmental pressure on the patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Metabolic markers of stress-induced myocardial ischemia.

The human heart in the fasting state extracts free fatty acids (FFA), glucose, lactate, pyruvate, and ketones from circulating blood. The utilization of FFA accounts for most of the oxygen consumed and energy produced at rest. Patients with angiographically demonstrable coronary artery disease and stable angina pectoris have a resting myocardial metabolism similar to that of normal individuals. During atrial pacing in normal persons, there is a significant enhancement of glucose uptake but that of FFA is unchanged, and the oxidation of carbohydrates accounts for more than 60% of the energy produced. In patients with stable angina, myocardial perfusion becomes regionally inadequate during stress. Despite the increase of myocardial glucose utilization, carbohydrate oxidation is negligible. Pyruvate will not be oxidized but in the presence of increased amounts of reduced coenzymes will be reduced to lactate. In addition, a greater amount of alanine will be released by the myocardium through the transamination of pyruvate, with a concomitantly greater uptake of glutamate that serves as the NH2 donor. In addition, glutamate may be used as an anaerobic fuel through conversion to succinate coupled with GTP formation. Although coronary hemodynamics, including myocardial perfusion, return to baseline within a few minutes after stress, a longer time course is needed for myocardial metabolism to become normal. In particular, myocardial utilization of exogenous glucose remains higher well after the normalization of hemodynamic parameters. This is more pronounced in postischemic myocardium, but it also occurs in nonischemic muscle, and glucose is presumably used for rebuilding glycogen stores that were depleted during ischemia.

Biomarkers↗
PubMed1990

[Comparison of lidoflazine and quinidine in the conversion to sinusal rhythm in atrial fibrillation of recent onset].

In order to compare the efficacy of oral lidoflazine (240 mg/die) and oral quinidine (1200 mg/die) in re-establishing sinus rhythm, we studied 115 patients (mean age 63.8 years; range 32-91) with atrial fibrillation of recent onset (less than 3 months). Patients with cardiac failure, acute myocardial infarction, severe intraventricular conduction disturbances, kaliemia less than 3.8 mEq/L or digoxinemia greater than 2 ng/ml were not included. Patients were randomly given one of the 2 drugs, until conversion to sinus rhythm was achieved, severe side effects occurred or for a maximum therapy of 5 days. No significant differences were present between the 2 groups in terms of age, male/female ratio, duration of atrial fibrillation, presence of an enlarged left atrium, presence of organic heart disease (or arterial hypertension) or digitalis therapy. Sinus rhythm resumption was obtained in 41/58 (71%) patients treated with quinidine and in 47/57 (82%) patients treated with lidoflazine (p = ns). In successful cases, the mean treatment time was 79 +/- 33 (SD) hours for quinidine and 66 +/- 36 hours for lidoflazine (p = ns). Both drugs showed the same efficacy in 3 subgroups of patients in whom the arrhythmia had different duration (less than 24 hours; between 24 hours and 3 days; more than 3 days). Treatment was stopped in 5 patients receiving quinidine (gastrointestinal side effects) and in 3 patients receiving lidoflazine (frequent premature ventricular beats in 2 and polymorphic ventricular tachycardia of the "torsade de pointes" type in 1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Forearm vasodilatory capacity in patients with syndrome X: a comparison with normal and hypertensive subjects.

Minimal forearm vascular resistances during maximal postischaemic vasodilation were measured in normotensive subjects with syndrome X, a condition characterized by angina and normal coronary arteries, in which a reduced coronary and systemic vasodilatory capacity has been reported. Age- and sex-matched normals and essential hypertensives constituted the control groups. The syndrome X patients had a significantly higher minimal forearm vascular resistance than the normals, indicating that arteriolar alterations may occur in the normotensive state and therefore cannot be considered solely as a consequence of hypertension.

Angina Pectoris↗
PubMed1989

Coronary hemodynamics and myocardial metabolism during and after pacing stress in normal humans.

We investigated coronary hemodynamics, myocardial utilization of circulating substrates (by coronary sinus catheterization), and overall use of oxidative fuels (by regional indirect calorimetry) in healthy adults during incremental atrial pacing (up to 159 +/- 9 beats/min), and during 25 min of recovery. Great cardiac vein flow (thermodilution) increased from 52 +/- 9 to 115 +/- 15 ml/min (P less than 0.001) with pacing; myocardial O2 uptake (301 +/- 53 to 593 +/- 71 mumol/min, P less than 0.001) and CO2 production (225 +/- 37 to 518 +/- 66 mumol/min, P less than 0.005) paralleled the pacing-induced rise in rate-pressure product (9.4 +/- 0.9 to 21.1 +/- 1.1 mmHg.beat. min-1.10(-3), P less than 0.001). During recovery, all the above variables returned to base line within 5 min, but myocardial O2 extraction remained depressed (67 +/- 2 vs. 71 +/- 3%, P less than 0.05). Circulating glucose uptake rose linearly with pacing (P less than 0.05) and remained above base line throughout recovery. By contrast, free fatty acid (FFA) uptake (10 mumol/min) did not increase with pacing and fell during recovery (P less than 0.01). Calorimetry, however, showed that net lipid oxidation exceeded FFA uptake throughout the study, whereas net carbohydrate oxidation was small at base line, rose significantly at maximal pacing (62% of myocardial energy output), and remained above base line during recovery (32% of energy output). In the basal state as well as during recovery, myocardial uptake of glucose equivalents (lactate plus glucose plus pyruvate) was in excess of carbohydrate oxidation, indicating nonoxidative disposal of these substrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗