[Etiopathogenesis of acute myocardial infarction: role of early leukocytosis]. / Eziopatogenesi dell'infarto miocardico acuto. Ruolo della leucocitosi precoce.

It has recently been suggested that inflammation may play an important role in the pathogenesis of acute ischemic syndromes. It may therefore be important to relate their clinical features with plasma indexes of inflammation. We have studied leukocyte, platelet and fibrinogen blood levels in 57 consecutive patients with acute myocardial infarction admitted to our Intensive Care Unit within 90 min after the onset of chest pain and treated with primary coronary angioplasty. Patients were divided into two groups on the basis of blood leukocyte levels: Group A, 24 patients, 17 males, mean age 54.2 +/- 13.7 years, with high blood leukocytes and Group B, 33 patients, 28 males, mean age 60.9 +/- 10.3 years, with normal blood leukocytes. Group A patients also had higher serum fibrinogen (p = 0.05) and blood platelet levels (p < 0.05). The stenosis observed after guidewire advancement was significant (> 75%) in 33% of the patients with leukocytosis vs 94% of the others (p < 0.01). No difference between the two groups was observed in the success rate of coronary angioplasty and prevalence of stent placement (100 vs 97%, and 43 vs 42% of the patients of Group A and B, respectively). In contrast, a tendency to rethrombosis requiring Rheopro administration was observed in 62% Group A patients vs 21% Group B patients (p < 0.01). In conclusion, the finding of leukocytosis in the acute phase of myocardial infarction suggests that coronary occlusion is mainly caused by a coronary thrombus occurring at the site of a non significant stenosis. In contrast, when blood leukocytes are normal, the underlying coronary stenosis is more often critical and the thrombotic process is less important. The high blood leukocytes, platelet and fibrinogen levels of Group A patients are consistent with a significant role of inflammation in the pathogenesis of the thrombotic process while hemodynamic and local mechanical factors are probably more important in patients with normal blood leukocytes.

[Evolution in coronary stenting: use of ticlopidine with and without oral anticoagulants]. / Evoluzione nel trattamento dello "stenting" coronarico: utilizzo della ticlopidina con o senza anticoagulanti orali.

Implantation of intracoronary stents has been rapidly increasing in the last few years, especially after a reduction of restenosis has been shown. The main limitation in the use of coronary endoprosthesis is still represented by acute and subacute thrombosis. In order to limit this dangerous complication a very strong coagulant regimen, which has been improved since 1993-94, was initially recommended. We report our experience with patients who underwent a stent implantation comparing two therapeutic regimens with or without oral coagulants associated with antiplatelet agents. During 700 consecutive coronary angioplasties 128 Palamatz-Schatz and Wiktor stents have been implanted in 118 patents (16.9%). After stent implantation, 33 patients underwent a traditional anticoagulant therapy with heparin followed by oral anticoagulants for 3 months. They were also treated with ticlopidine 250 mg/die started 2 days before the procedure and then kept at least one month (group A). Eighty-five patients were treated only with antiplatelet therapy (ticlopidine 500 mg/die) started 2 days before implantation (group B). These two groups of patients were similar in age, sex, type and number of treated vessels and in diameter of the vessel with stent implantation. Subacute thrombosis rate was not significantly different between groups (3 vs 2.3%, NS). The predictive factors of thrombosis were acute myocardial infarction and implantation of multiple stents. No significant differences were found between thrombosis of the stents implanted in bail-out conditions compared to the elective ones. Ticlopidine started 2 days before stent implantation seems to be sufficient to limit thrombosis rate; moreover it allows a reduction of the hemorrhagic complications and hospitalization period.

[Ischemic cardiopathy in the young: coronarographic and autopsy picture in 100 subjects]. / La cardiopatia ischemica nel giovane: quadro coronarografico ed autoptico in 100 soggetti.

Many aspects of coronary artery disease in young people are not completely understood. Our study concerns a series of 100 patients < 45 years with acute coronary artery disease. Sixty patients survived and 40 died suddenly. All subjects have been divided into four groups: Group I includes 20 deceased patients with anatomic features of acute myocardial infarction. Group II includes 20 subjects dead without features of acute myocardial infarction. Group III includes 30 patients surviving the first acute myocardial infarction. Group IV includes 30 patients surviving unstable angina. The coronary arteries have been studied by anatomic dissection in Group I and II and with coronarography in Groups III and IV. The left main was only involved in Group I and II patients. Multivessel disease was more frequent in Group I and II, but the difference was not significant. These results underline that coronary artery disease with multivessel involvement is not rare in young patients. The rare occurrence of left main disease at coronary angiography could be the consequence of the natural preselection determined by sudden death.

Combined invasive and noninvasive study of left ventricular systolic and diastolic function following acute administration of cicloprolol to subjects with normal cardiac function.

Cicloprolol is a new beta-blocking agent with high selectivity for beta 1 receptors and high intrinsic sympathomimetic activity. We studied the acute hemodynamic effects of cicloprolol in nine subjects with no evidence of left ventricular dysfunction who underwent cardiac catheterization for the evaluation of chest pain. All patients had normal coronary angiography and left ventriculography. Left ventricular pressure was determined throughout the cardiac cycle using a Millar 8Fr Minotip catheter; an echocardiogram, phonocardiogram, and ECG were simultaneously recorded to obtain left ventricular pressure-diameter loops. All the measurements were repeated before and after the intravenous administration of cicloprolol. Cicloprolol was administered at increasing doses of 0.05, 0.10, and 0.25 mg/kg until a cardiac output increase of at least 15% over basal values was achieved. A decrease of mean arterial pressure or cardiac output after cicloprolol was not observed in any patient. Cicloprolol administration significantly increased cardiac output (24%), stroke volume (22%), and peak positive dP/dt (25%); no significant changes in heart rate, systemic blood pressure, right atrial pressure, or pulmonary artery pressures were observed. No significant change in the echocardiographic parameters occurred. Among the indices of left ventricular diastolic function, the time constant of isovolumetric relaxation was significantly decreased (-43%) after cicloprolol; moreover, the left ventricular pressure-diameter loop in the protodiastolic phase was shifted to the left following cicloprolol infusion. This study confirms that in subjects with normal left ventricular function cicloprolol can improve resting left ventricular systolic function, and it shows that this action can also be attended by a more rapid isovolumetric relaxation, similar to what has been observed with other sympathomimetic amines.

Morbidity and mortality of patients with sinus node disease: comparative effects of atrial and ventricular pacing.

In patients with sinus node disease (SND), VVI pacing seems an inappropriate method of cardiac stimulation because of its potential adverse hemodynamic and arrhythmic effects. AAI-DDD pacing, preferred because of lower morbidity, may also determine a higher survival rate. We examined retrospectively two groups of patients with SND. Stimulated respectively with VVI pacing (group 1 = 57 patients) and AAI pacing (group 2 = 53 patients). The mean duration of the follow-up interval was 40.1 months for group 1 and 45 months for group 2. Ten patients (17.5%) in the VVI group and five (9.4%) in the AAI died. During the follow-up, in the VVI group three patients developed congestive heart failure and ten developed chronic atrial fibrillation, whereas only one case of heart failure and two with atrial fibrillation have been recorded in the AAI group. Moreover, four patients had embolic complications in group 1. Five patients (9.4%) with AAI pacing were converted to sequential pacing due to the occurrence of second-degree heart block. The statistical analysis was developed by the X2 test for the comparison of the proportion of the events (atrial fibrillation, congestive heart failure, embolic accidents) in the two groups: a significantly higher morbidity (P less than 0.01) was recorded in the AAI group. Survival is also higher in AAI patients, but the survival rate difference, calculated using the Mantel-Cox method, is not statistically significant. The findings of our study show that in SND the superiority of AAI pacing over VVI is statistically significant as far as morbidity is concerned, and we have also noticed an evident but not statistically significant superiority regarding mortality.

[Percutaneous coronary transluminal angioplasty with extracorporeal circulation: preliminary results]. / Angioplastica coronarica percutanea transluminale con assistenza circolatoria extracorporea: risultati preliminari.

Percutaneous transluminal coronary angioplasty (PTCA) in patients with low ejection fraction (EF) and/or a large area of remaining viable myocardium served by the target vessel can cause hemodynamic collapse in case of acute closure. We report 11 patients in whom the cardiopulmonary bypass support (CPS) was instituted because of contraindication to surgery (Group I) or unstable angina associated with low EF and/or a large amount of myocardium perfused by the target artery (Group II). Nine were male and 2 female, mean ages of 70, with Canadian angor class I (1), II (1), or IV (9) and EF ranging from 12 to 65% (mean 34%). Thirty were the lesions to dilate; 28 were dilated successfully; in 2 an aortic dilation was also performed. One death occurred after the procedure related to collapse due to hypovolemia; another death occurred 8 months after PTCA because of pulmonary neoplasia. The other 9 patients followed-up at 1 to 8 months (mean 3.9) disclosed Canadian angor class I. The procedure's technique and the related complications are discussed. We conclude that cardiopulmonary bypass support can be used safely in patients refused to surgery and with high risk PTCA; such a procedure may expand the indication of PTCA.

SWAT team approach to ventricular assistance.

In 1986, the Cardiovascular Research Institute in Sion, Switzerland, created a flying bridge-to-cardiac transplantation team. This team, consisting of two physicians, a physicist, a biomedical engineer, and two intensive care nurses, has participated in 23 bridges to cardiac transplantation in 11 cardiovascular surgery centers in Europe. The cardiac function of all patients was 100% supported by paracorporeal pneumatic biventricular Pierce-Donachy devices. Twenty of the 23 patients have had transplantation, and 11 are alive and well. The bridge-to-cardiac transplantation team, which travels with a transportable driver and the ventricle sets, supervises the bridged patients 24 hours a day until cardiac transplantation is performed.

A randomized double-blind crossover study of nicardipine and nifedipine in patients with angina pectoris and concomitant essential hypertension.

The two dihydropyridine calcium antagonists, nicardipine and nifedipine, were compared in 12 patients with both stable angina pectoris and systemic hypertension using a double-blind, crossover protocol. After a 2-week placebo run-in period, each patient was randomized to either nicardipine or nifedipine; each drug was titrated up to either blood pressure normalization, appearance of adverse effects, or maximal dosage (40 mg, three times a day with nicardipine and 30 mg, three times a day with nifedipine) and then administered for 4 weeks. Maximal symptom-limited exercise tests were performed at the end of the placebo run-in and each treatment period, 3 and 8 hours after drug administration. Nicardipine and nifedipine were used at the mean doses of 100 +/- 20 mg/day and 57 +/- 20 mg/day, respectively. Both drugs reduced, significantly and similarly, standing and supine blood pressure, frequency of anginal episodes, and nitroglycerin consumption. At 3 hours after drug administration, exercise duration and time to 1-mm ST depression increased significantly from 402 +/- 84 and 306 +/- 108 seconds, respectively, with placebo; to 533 +/- 135 and 442 +/- 138 seconds during nicardipine; and to 518 +/- 118 and 437 +/- 133 seconds during nifedipine, with a concomitant reduction of peak ST depression. Both submaximal and maximal exercise diastolic blood pressure were significantly reduced by the two calcium antagonists whereas systolic blood pressure was decreased only at submaximal but not at maximal exercise; the heart rate was not significantly modified by the two drugs at any exercise stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Late systolic stress-diameter relation in patients with aortic valve disease before and after valve replacement.

The end-systolic pressure-diameter ratio (Ees) and the maximal pressure-diameter ratio (Emax) during systolic ejection were determined in 10 control patients and 25 patients with aortic valve disease before and 18 months after successful valve replacement. The pressure-diameter ratio was determined from simultaneous M-mode echocardiograms and high-fidelity pressure measurements. A new index of myocardial contractility, as proposed by Pouleur and co-workers, was assessed from the late systolic stress-diameter relationship during one single heart cycle. The slope of this stress-diameter relationship was used for determination of myocardial contractility. Meridional wall stress was calculated from echo-pressure measurements at time intervals of 5 to 10 msec. The aortic valve patients were divided into two groups according to the preoperative angiographic ejection fraction: group 1 (ejection fraction greater than or equal to 57%) consisted of 16 patients and group 2 (ejection fraction less than 57%) of 9 patients. Standard hemodynamics showed a significant decrease in left ventricular end-diastolic pressure from 18 to 11 mm Hg in group 1 (P less than 0.01) and from 16 to 12 mm Hg (NS) in group 2. Peak systolic pressure decreased from 186 to 135 mm Hg (P less than 0.01) in group 1 and from 155 to 140 mm Hg (NS) in group 2. Left ventricular end-diastolic volume decreased from 137 to 105 ml/m2 in group 1 and from 225 to 150 ml/m2 in group 2 (P less than 0.05) whereas left ventricular ejection fraction remained unchanged in group 1 (67 versus 65%) and increased slightly in group 2 (45 versus 51%) following surgery. Emax and Ees were preoperatively significantly decreased in group 2 when compared to group 1. Postoperatively, Emax and Ees were no longer significantly different between the two groups although left ventricular ejection fraction remained significantly depressed in group 2 after surgery when compared to group 1. The slope of the late systolic stress-diameter relationship (beta) and the diameter at zero stress (D0) did not show any difference between the two groups pre- as well as postoperatively. Thus it is concluded that Ees and Emax might help to identify myocardial dysfunction in preoperative patients with aortic valve disease. However, in the presence of persistent myocardial dysfunction, as evaluated from systolic ejection fraction, following successful valve replacement, both Ees and Emax do not allow to identify patients with postoperative depressed myocardial function.(ABSTRACT TRUNCATED AT 400 WORDS)

[Relaxation and regional myocardial stiffness in obstructive hypertrophic cardiopathy patients: effect of verapamil]. / Rilassamento e stiffness miocardica regionali in pazienti affetti da cardiomiopatia ipertrofica ostruttiva: effetto del Verapamil.

Diastolic stiffness of the septum and the posterior wall were determined in 6 patients with hypertrophic obstructive cardiomyopathy before and 10 to 15 min after the intravenous administration of verapamil, 0,1 mg/kg. Left ventricular high-fidelity pressure measurements and M-mode echocardiography were carried out in all patients before and after verapamil. Diastolic stiffness of the septum (beta S) and of the posterior wall (beta) were assessed from the slope of a viscoelastic stress-strain relationship: sigma = alpha (e beta epsilon -1) + eta epsilon where sigma = meridional wall stress (g/cm2) alpha = intercept (g/cm2), beta = constant of myocardial stiffness, epsilon = mid-wall strain, eta = constant of myocardial viscosity (g. sec/cm2), epsilon = strain rate (sec-1). Left ventricular relaxation was evaluated from the time constant of left ventricular pressure fall (T; msec) by plotting left ventricular pressure versus dP/dt during the isovolumic relaxation period. Heart rate (71 versus 74 beats/min), left ventricular end-diastolic pressure (17 versus 17 mmHg) and peak systolic pressure (152 versus 146 mmHg) were not significantly different before and after intravenous administration of verapamil. The constant of myocardial wall stiffness of the septum (17 versus 16) and the posterior wall (15 versus 13) remained unchanged after verapamil, however, myocardial stiffness of the septum was slightly higher than myocardial stiffness of the posterior wall. The time constant of left ventricular pressure fall decreased significantly (P less than 0.05) from 53 to 43 msec following administration of verapamil. It is concluded that in patients with hypertrophic, obstructive cardiomyopathy, diastolic myocardial stiffness of the septum is slightly higher than the stiffness of the posterior wall. Verapamil does not influence the regional passive diastolic properties but has a beneficial effect on ventricular relaxation.