Percutaneous bridge to heart transplantation by venoarterial ECMO and transaortic left ventricular venting.

We report a case in which life support for cardiogenic shock was achieved by a nonpulsatile venoarterial bypass, and left ventricular decompression was obtained by a catheter placed percutaneously through the aortic valve into the left ventricle. The blood drained from the left ventricle was pumped into the femoral artery. The normalization of left heart filling pressures allowed the resolution of pulmonary edema, and the patient underwent a successful heart transplantation following 7 days of mechanical cardiocirculatory support.

Three weekly injections (TWI) of low-dose growth hormone (GH) restore low normal circulating IGF-I concentrations and reverse cardiac abnormalities associated with adult onset GH deficiency (GHD).

GH replacement therapy given 3 times weekly (TWI) and adjusted to allow serum IGF-I concentrations in the mid-normal range for sex and age has been shown to be as effective as the daily regimen in improving lipid profile, body composition, bone mass and turnover in adult GH deficient (GHD) patients. Only one study has investigated so far the short-term (6 months) effect of a fixed weight-based TWI dosing schedule on heart structure and function in childhood onset (CO) GHD patients, whereas such a schedule in adult onset (AO) GHD patients has not been studied as yet. Aim of this study was to investigate whether a 1-yr low-dose titrated TWI GH-replacement regimen aimed at achieving and maintaining IGF-I levels within the low normal limits for age and sex is able to affect cardiovascular and heart parameters in a group of AO GHD patients. Eight adult patients (4 women and 4 men, age 35.8 +/- 3.37 yr, body mass index, BMI, 28.7 +/- 2.62 kg/m2) with AO GHD were included in the study, along with 10 healthy subjects, matched for age, sex, BMI and physical activity (6 women and 4 men, age 35.2 +/- 4.05 yr, BMI 28.4 +/- 2.34 kg/m2). M- and B- mode ecocardiography and pulsed doppler examination of transmitral flow were performed in GHD patients at baseline and after 3 and 12 months of GH therapy (mean GH dose 6.7 +/- 0.8 microg/kg/day given thrice a week), while normal subjects were studied once. Treatment with GH for 1 yr induced a significant increase in left ventricular (LV) diastolic and systolic volumes (+11.1 and +16.5%, respectively). Systolic LV posterior wall thickness and LV mass were increased (+10.2 and +7.7%, respectively) by GH administration. Systemic vascular resistance was significantly decreased by 1-yr GH therapy (-13.8% after 1 yr), while stroke volume, cardiac output and cardiac index were increased (+9.4, +11.6 and + 11.9%, respectively). LV end-systolic stress was decreased at the end of GH therapy (-11.2%). E and A wave, significantly reduced at baseline, were increased by 1 yr of GH therapy (+23.3% and +28.1%, respectively); likewise, the abnormally high E peak deceleration time was partially reversed by GH administration (-10.7%). Our study, though conducted in a small sample size, demonstrates that a TWI GH treatment schedule is able to reverse the cardiovascular abnormalities in AO GHD patients and to improve body composition and lipid profile. The maintenance of circulating IGF-I concentrations within the low normal range allows to avoid most of the side-effects reported with higher GH doses while being cost-effective and improving the patient's compliance.

Echocardiography-guided pericardiocentesis with probe-mounted needle: report of 53 cases.

Fifty-three pericardiocentesis procedures were performed on 48 patients from 1993 to 2000 at our coronary care unit. Percutaneous puncture (anterior thoracic in 43 cases, subxiphoid in 10 cases) was performed at the site closest to the exploring probe, where the largest amount of fluid was detected. A needle carrier supported by a bracket with two fixed angulations was mounted on the probe. The needle was advanced through the tissues and inside the pericardial space under continuous visualization. The procedure was successful in 52 of 53 cases. In 1 case of diagnostic pericardiocentesis, the pericardial space was impossible to reach because of the minimal amount of pericardial fluid. In 1 case of acute tamponade after transcatheter ablation of the atrioventricular node, the pericardial puncture caused a pleural-pericardial shunt with consequent drainage of pericardial fluid into the pleural space and symptom resolution. In 1 case, a transient atrioventricular type III block occurred. Emergency surgical drainage was not required in any of the cases. No puncture of cardiac walls ever occurred in this series of patients. No major complications occurred; the incidence of minor sequelae was lower than the incidence reported by other studies on pericardiocentesis without continuous visualization. Our technique appears to be safe and easy to perform even in the presence of minimal amounts of pericardial fluid.

Time course of circulatory and humoral effects of rapid total paracentesis in cirrhotic patients with tense, refractory ascites.

BACKGROUND/AIMS: Tense ascites of cirrhosis can be treated with total paracentesis; however, the short-term effects of this procedure are poorly defined. METHODS: The circulatory and humoral changes induced by total paracentesis (250 mL/min) were studied in 12 cirrhotics with tense, refractory ascites. Data were collected before, during, and after paracentesis and 24 hours later (after albumin infusion). Hormonal parameters were recorded again 48 hours and 6 days thereafter. RESULTS: Paracentesis (10.7 +/- 4.4 L; 64 +/- 20 minutes) caused marked reduction of intra-abdominal, intrathoracic, right atrial, and pulmonary pressures. Heart rate did not change. Cardiac output and heart volumes increased. Systemic vascular resistances and mean arterial pressure slightly decreased. Baseline plasma renin and aldosterone levels were markedly increased; a reduction was already evident during paracentesis with the lowest values at the end of the procedure. All changes were maintained 24 hours later. Hormones regained baseline levels 6 days later. CONCLUSIONS: Rapid total paracentesis is accompanied by marked cardiovascular and humoral changes. Some of these changes can be explained by mechanical factors that are directly or indirectly related to the relief of abdominal pressure. However, other changes (systemic vasodilatation, humoral deactivation) have a non-mechanical nature and may depend on reflexes originating from cardiac volume receptor stimulation. Most changes may beneficially (albeit transiently) influence the cardiovascular system of cirrhotic patients with tense ascites.

Cardiopulmonary receptor and arterial baroreceptor reflexes after acute myocardial infarction.

The baroreceptor-heart rate reflex in human is impaired 2 days after a myocardial infarction but it improves 10 days after the acute coronary event. This study investigated whether (1) the baroreceptor-heart rate reflex improvement takes the reflex back to normal, and (2) the cardiopulmonary reflex is affected by myocardial infarction. In subjects studied 8 to 11 days after a transmural anterior or inferior myocardial infarction the baroreceptor-heart rate reflex sensitivity (slope of the linear regression between negative neck chamber pressures and lengthenings in RR interval) was similar to that seen in control subjects (-6.2 +/- 0.8 vs -6.0 +/- 0.6 ms/mm Hg, mean +/- SEM) and did not change when reassessed 10 days later. In contrast, the cardiopulmonary reflex sensitivity (changes in forearm vascular resistance induced by changing central venous pressure through nonhypotensive lower body suction and leg raising) was markedly less in subjects studied 8 to 11 days after myocardial infarction than in control subjects; the reduction amounted to 58.1 +/- 8% (p less than 0.01). The cardiopulmonary reflex sensitivity greatly improved when reassessed 28 to 45 days later. Thus, the baroreflex is normal about 10 days after myocardial infarction. This condition markedly impairs the cardiopulmonary reflex, but the impairment is also transient.

[Cardioangioimmunology: the immune implications in the principle cardiovascular pathologies]. / Cardio-angio-immunologia: implicazioni immunitarie nelle principali patologie cardiovascolari.

At present, it is known that the immune system acts through the release of protein factors, so-called cytokines. In addition to their immunomodulating and endocrinometabolic effects, cytokines have appeared to be able to have an influence on the cardiovascular system by inducing important haemodynamic changes. Cytokines cause hypotension, particularly IL-2 and TNF, due at least in part to a production of nitric oxide by endothelial cells. Cytokines, such as IL-1, IL-6 and TNF, stimulate myocardial infiltration by activating leukocytes and inducing the release of cytotoxic factors during myocardial infarction; that would extend the area of necrosis. Finally, cytokines would be involved in the pathogenesis of the atherosclerosis, and cholesterol metabolism itself would be under a cytokine control. On these bases, it is possible to suggest in the near future the elaboration of new therapeutic strategies and prognostic indications, according to the bioimmunological response of patients with cardiovascular diseases.

Early alterations of the baroreceptor control of heart rate in patients with acute myocardial infarction.

Experimental coronary occlusion is accompanied by an acute impairment of the baroreceptor-heart rate reflex. This study was planned to determine whether this impairment also occurs in humans. In 30 patients admitted to a coronary care unit for an anterior (n = 14) or inferior (n = 16) transmural myocardial infarction (MI), we measured 1) the increase in RR interval induced by stimulating carotid baroreceptors through progressive reductions in neck chamber pressure, 2) the increase in RR interval induced by stimulating arterial baroreceptors through intravenous boluses of phenylephrine, and 3) the reduction in RR interval induced by deactivating arterial baroreceptors through intravenous boluses of nitroglycerin. Measurements were performed 49.5 +/- 2.4 hours (mean +/- SEM) after the MI. The results were compared with those of five age-matched patients admitted to the coronary care unit for chest pain and found free from ischemic heart disease. The sensitivity of the carotid baroreceptor-heart rate reflex (slope of the linear regression of RR interval over neck pressure changes) was markedly less in MI than in control patients (3.8 +/- 0.5 vs. 5.9 +/- 0.6 msec/mm Hg, p less than 0.05), the reduction being similar in patients with anterior and inferior MI. This was the case also for the baroreflex sensitivity measured by the phenylephrine and the nitroglycerin methods (slope of the linear regression of RR interval over systolic blood pressure changes). However, 10.2 +/- 0.3 days later, the baroreflex sensitivity measured by all three methods increased significantly (p less than 0.05 or 0.01) and became similar to that of control subjects, which showed no significant change from the early to the late period after admission into the coronary care unit. Thus, MI is accompanied by an acute marked impairment of the baroreceptor control of the heart in humans, and this is the case both for an anterior and an inferior MI. The impairment is largely transient in nature, however, and a clear-cut recovery of the baroreflex can be seen a few days later.

Effects of digoxin, placebo and ibopamine on exercise tolerance and cardiac rhythm of patients with chronic post-infarct left ventricular failure.

This study compares the effects of digoxin, placebo and ibopamine (SB-7505), the orally active 3,4-diisobutyryl ester of N-methyl-dopamine, on exercise tolerance and cardiac rhythm of 14 patients whose left ventricular heart failure (end-diastolic pressure, 26.3 +/- 5.9 mmHg; ejection fraction, 0.42 +/- 0.10%) depended on a previous myocardial infarction. Patients were admitted to the study while on chronic oral digoxin treatment (serum levels between 1.1 and 1.9 ng/ml). Placebo instead of digoxin was given for the following month. Thereafter ibopamine 50 mg t.i.d. for one month was given. A sequence of one-month treatments with digoxin, placebo and ibopamine was repeated, then ibopamine was administered continuously for the next two months. The concurrent treatment (diuretics in all patients, nitroderivates in twelve, calcium antagonists in two) remained unchanged during the observation period. Symptoms-limited exercise tests and 24-h Holter recordings were obtained at admission, at the end of each one-month treatment and at the end of the observation period. Two patients developed unstable angina without increase of serum creatine phosphokinase while on ibopamine and were withdrawn. Out of the 12 patients that concluded the trial, one required supplementary doses of diuretic at the end of the second period on placebo. The results obtained during the trial suggest that: a) therapeutic plasma levels of digoxin have no deleterious effect on cardiac rhythm nor significantly increase exercise tolerance as compared with placebo; b) diuretics and nitrates appear to sustain the clinical stability of these patients as a group.(ABSTRACT TRUNCATED AT 250 WORDS)