[How to use and improve DRG: role of the cardiologist].
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Biomedical subjects
Publications and source records attributed to G Pinelli.
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Therapy of patients presenting with cardiogenic shock refractory to medical treatment can be undertaken with uni or biventricular circulatory assist devices. Pre implantation evaluation of patients is aimed at defining the etiology as well as the extent of uni versus biventricular heart failure, the possibility of recovery of myocardial function improvement of vital organ function and the possibility of cardiac transplantation. Circulatory assist devices must provide efficient support of the failing ventricles, allow recovery of myocardial function or cardiac transplantation under optimal circumstances. The choice of uni-biventricular support of total artificial heart is discussed as well as criteria useful in defining a therapeutic strategy.
The efficiency of a number of tertiary treatment systems--filtration, ozonation, chlorination with low levels (TRC < 0.2 ppm) and high levels (TRC < 1 ppm) of residual chlorine--in the disinfection of secondary effluent was assessed in a purification plant treating mixed sewage of municipal (83%) and industrial mainly textile origin (17%). Maximum purification effect was observed when, following secondary treatment with biological oxidation, the sewage was submitted to combined filtration--ozonation treatment (reduction in bacterial indicators of from 4.9 to 7.2 log10 units) or with chlorination with high levels of residual chlorine (reduction in the bacterial indicators of between 2.8 and 4.6 log10 units). However, only ozonation reduced viral indicators with respect to inflow sewage by more than 3 log10 units, the limit considered acceptable for a biological treatment system with supplementary tertiary disinfection treatment. Ozonation however did not complete control all the biological forms present in the sewage, in particular the viruses, present in 36% of ozonized samples at concentrations of from 1 to 480 PFU/100 mL. Ozonation and high-concentration chlorination do not seem to be unfavorably influenced by wastes from laundry and deyng processing; achieving a complete decolorization of the treated effluent, they prove to the suitable treatments for mixed sewage of municipal and industrial mainly textile origin.
This study compares the incidence and management of acute closure complicating coronary angioplasty in three historic populations of patients having undergone the procedure at the same center: group 1 (n = 146 of 881) ("early years" of angioplasty, 1980 to 1986), group 2 (n = 113 of 1781) (bailout stenting learning curve, 1990 to 1992), and group 3 (n = 34 of 525) (1993). The incidence of acute closure decreased from group 1 (146 [17%] of 881) to groups 2 and 3 (147 [6%] of 2306); (p < 0.001). Management of the occlusion changed over the years, with less emergency coronary bypass surgery ([36%] 52 of 146, 15 [13%] 113, and 3 [9%] of 34), respectively, p < 0.01) and more repeat angioplasty (70 [48%] of 146; 87 [78%], of 113, and 30 [88%] of 34, p < 0.001). The use of prolonged inflations (> 10 minutes) and stenting increased from group 2 (15 [13%] of 113 and 16 [14%] of 113, respectively) to group 3 (12 [35%] of 34, and 10 [30%] of 34, respectively). In-hospital death occurred in 18 (12%) of 146, 7 (6%) of 113), and (2 (6%) of 34) patients in the three groups. Acute myocardial infarction decreased from 64% to 46% and 27%, respectively (p < 0.01). Overall, the number of patients free of events at hospital discharge increased from 38 (26%) of 146 to 53 (47%) of 113 (p < 0.001) and to 23 (68%) of 34 (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Because of problems concerning the functional quality of heart transplants, more and more interest has been focused on the physiologic changes occurring during brain death, one of the major possible contributing factors to the myocardial alterations. METHODS: The aim of this study was to describe the link between acute experimental brain death and myocardial metabolism. This was achieved by in vivo 3-hour hemodynamic and biological (myocardial lactate production) studies and then in vitro 6-hour phosphorus-31 nuclear magnetic resonance spectroscopy. Two groups of pigs were involved in the study: group I (n = 10) as control and group II (n = 10) as brain-dead animals. RESULTS: Within the first hour, we observed a strong increase in myocardial activity associated with the onset of myocardial lactate production, lasting 2 hours and corresponding to a myocardial anaerobic metabolism period. Despite the apparent normalization before excision of the hearts, phosphorus-31 nuclear magnetic resonance spectroscopy revealed a significant decrease in adenosine triphosphate levels in group II when compared with group I. CONCLUSIONS: We conclude that, in our study, acute experimental brain death is associated with an early and transient period of myocardial anaerobic metabolism and adenosine triphosphate consumption. These myocardial consequences of brain death could partially explain some observations of heart graft dysfunction.
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BACKGROUND: Mechanisms precipitating sudden death are poorly known, in spite of the importance to detect functional factors which may contribute to such fatal event. Aim of the study was to investigate the relationship between "ischemic" sudden death (ISD: arrhythmic death preceded by acute myocardial ischemia) and autonomic nervous system activity. METHODS: We analysed the tapes of 6 patients (pts) (5 males; 67 +/- 12 yrs) suffering ISD during Holter monitoring (HM). One pt had recent onset angina, 2 had unstable and 3 stable angina; none was taking antiarrhythmic drugs. Arrhythmias, ST segment and heart rate variability (HRV) were analysed by a computerized interactive HM system, in order to obtain data on transient ischemia and sympatho-vagal balance. RESULTS: Five pts showed ventricular tachyarrhythmias (2 VF, 3 VT), and 1 had a bradyarrhythmia (advanced A-V block) as the terminal event; all pts showed ST shift (max: 0.37 +/- 0.28 mV; 1 with ST elevation; 4 with anginal pain) 53 +/- 35 min before ISD. SD of normal R-R intervals (SDNN) was 112 +/- 26 msec in the 11 +/- 8 hrs of HM, whereas it was 97 +/- 48 msec in the initial hour and 59 +/- 21 msec in the initial 5 min segment. Measurements of SDNN showed a marked decrease 5 min before the onset of fatal ischemic ST shift: 32 +/- 14 msec (p = 0.003). Also, pNN50 (percent of adjacent R-R differing > 50 msec: marker of vagal activity) was significantly reduced before ISD, when compared to the initial 5 min segment (from 10 +/- 5 to 7 +/- 4%; p < 0.03). Such changes were not observed before uncomplicated (that is not associated with malignant arrhythmias) ST shift episodes during HM. CONCLUSIONS: Autonomic dysfunction, as detected by a marked decrease of HRV, is present in the period (5 min) immediately preceding the onset of ST shift precipitating ISD; simultaneous measurements of vagal signals showed similar changes. These data suggest that sympatho-vagal unbalance may trigger fatal arrhythmias during acute myocardial ischemia, hence resulting in ISD.
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Valvular tumors are uncommon and usually benign lesions, discovered accidentally or when neurological or cardiological complications occur. We report a case of mitral valve papillary fibroelastoma measuring less than 1 cm and revealed by stroke. Transesophageal echocardiography was the best method to establish the diagnosis as it provided higher discriminative power than the transthoracic echocardiography or nuclear magnetic resonance. The embolic risks justify the surgical treatment of these lesions while anticoagulation therapy can be suggested as a substitute to surgery for the high risk patients.
Between 1985 and 1992, the gastroepiploic artery was used for coronary bypass surgery in 80 consecutive patients. Revascularisation was totally arterial in 62.5% of cases, the gastroepiploic being associated with single or double internal mammary artery grafts. The gastroepiploic graft was used to revascularise the inferior myocardial regions. The postoperative morbidity was essentially due to respiratory complications: 6 patients had objective pulmonary complications and 11 patients had relative transient postoperative hypoxia. The early gastrointestinal complications were related to ulceration (5 patients) complicated by haemorrhage in 2 patients. This morbidity was responsible for a significant increase in the period of intensive care. The hospital mortality was 6.2%, observed mainly in the first third of the author's experience and in patients with preoperative poor prognostic factors. These relatively high morbidity and mortality rates have led to a cautious use of the right gastroepiploic artery for coronary bypass surgery in patients over 70 years of age, in those with unstable angina operated as an emergency and in those with associated pathology, especially respiratory problems. The choice of a complex surgical option should not be synonimous with an increased postoperative mortality.
Changes in hemodynamic and metabolic parameters (systemic oxygen delivery, [DO2], oxygen consumption [VO2], arterial lactate content) in brain-dead and control pigs in the absence of any inotropic or fluid support were studied. Brain death was induced by the inflation of a Foley catheter balloon placed into the subdural space of the animals. Serial atrial natriuretic peptide (ANP) determinations were performed to evaluate concomitant changes occurring in the endocrine function of the heart. Experiments were completed by a volume expansion protocol to provide a dynamic evaluation of these parameters. A significant increase in heart rate (from 113 +/- 5 to 176 +/- 11 beats/min), pulmonary capillary wedge pressure (from 7 +/- 1 to 12 +/- 3 mmHg), dP/dt (from 2040 +/- 340 to 4200 +/- 660 mmHg/sec-1), cardiac output (from 2.4 +/- 0.2 to 3.3 +/- 0.4 L/min), mean arterial pressure (from 66 +/- 8 to 93 +/- 14 mmHg), and systemic oxygen delivery (from 360 +/- 30 to 530 +/- 90 ml/min-1), was observed following brain death induction. These parameters returned below basal values within 60 min. On the contrary, serum lactate and VO2 remained unchanged. Following volume expansion, brain-dead pigs exhibited impaired hemodynamic response, with a significant decrease in dP/dt, MAP, and DO2. These changes were accompanied by a significant decrease in VO2 and a significant increase in lactate plasma levels. At the same time, a similar increase in ANP release was observed in both groups in response to volume expansion, suggesting that despite impaired myocardial contractility, endocrine function of the heart was preserved following brain death. We conclude that brain death leads to early impaired left ventricular contractility, which could be responsible for the changes observed in aerobic to anaerobic metabolism in response to rapid volume infusion. These results suggest that the use of fluid infusion to reduce the need in inotropic support in conventional therapeutic modalities should be used with care in the management of a brain-dead potential organ donor.
Brain death is a pathophysiological condition associated with major hemodynamic changes, temporary myocardial ischemia, and histological damage of the heart. These modifications could be related to a major local release of norepinephrine from myocardial sympathetic nerve endings leading to norepinephrine cardiotoxicity. This study was designed to evaluate the utility of cardiac microdialysis to measure interstitial myocardial norepinephrine release resulting from brain death. The dialysis probe consisted in a 10 x 0.20-mm dialysis fiber with a 18,000 mol wt cutoff. Dialysis probes were implanted into the right and left ventricular walls of the beating heart in anesthetized pigs and perfused with Ringer solution at 2 microliters/min. Dialysate norepinephrine concentration was measured using HPLC with electrochemical detection. The relative recovery rate of norepinephrine in vivo was 34 +/- 4%. Interstitial fluid concentrations were obtained using the following formula: [C]interstitium = [C]dialysate/Recovery in vivo. After brain death, a transient increase in interstitial norepinephrine concentration was observed (from 0.74 +/- 0.20 to 4.50 +/- 0.60 ng/ml and 0.76 +/- 0.20 to 6.2 +/- 0.9 ng/ml in left and right ventricle, respectively, P < 0.01) which far exceeded plasma level increase (from 0.50 +/- 0.10 ng/ml to 0.91 +/- 0.20 ng/ml, P < 0.05). This increase in myocardial norepinephrine was, moreover, biphasic, with a second peak occurring 40 min after brain death. The present study confirms the onset of a dramatic increase in cardiac norepinephrine release from myocardial nerve endings following brain death, and demonstrate the utility of the new cardiac microdialysis technique to assess changes in interstitial fluid content.
We examined 166 patients with advanced chronic obstructive pulmonary disease (COPD) treated with long-term oxygen therapy (LTOT) in order to evaluate the prognostic factors of such patients. The mean observation period was 24 months (range 2-50 months) and the following variables were considered: age, forced expiratory volume in 1 s (FEV1), arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), hematocrit, right ventricular systolic pressure (RVSP; evaluated by Doppler echocardiography), number of hospitalizations in the 2 years prior to prescription of LTOT and body mass index. The overall survival rate was 78.3% at 24 months and 67.1% at 36 months. A univariate analysis identified three variables as significant predictors of survival: FEV1, PaO2 and RVSP. A multivariate analysis, using Cox's model, showed an independent predictive power for RVSP, age and FEV1. RVSP higher than 35 mm Hg, age greater than 70 years and FEV1 lower than 30% of the predicted value were associated with shortened survival. The importance of pulmonary hypertension as a predictor of death suggests that LTOT could be prescribed earlier for COPD patients with cor pulmonale, as oxygen has been shown to be the only effective therapy for improving the survival probability of these patients.