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An 89-year-old female was referred to the authors' institution for repeating pulmonary edema. Recent transthoracic echocardiography (TTE) showed only a mild mitral regurgitation (MR), but a transient severe reversible functional MR was observed during an episode of respiratory distress. TTE demonstrated the functional nature of the regurgitation with a transient tenting of the mitral leaflets, resulting in a total absence of coaptation.

This study investigated the hemodynamic effects and tolerance of infusion of 10 micrograms/kg/min enoximone over 7 days in 12 patients (mean age 64.3 years) with severe chronic heart failure (10 NYHA Class III and 2 Class IV) with idiopathic dilated cardiomyopathy. Hemodynamic parameters were measured 10 minutes, 3 hours, 6 hours, 18 hours, 24 hours, and 7 days after the start of infusion. Catecholamines were assayed before the start of the infusion and on day 7. The heart rate increased on an average from 90.8 +/- 13.7 before infusion to 108.5 +/- 8.2 beats/min (p < 0.05) on day 7 (+20%). The mean arterial pressure decreased by approximately 10% (p < 0.05) between the start and end of the infusion. The pulmonary artery diastolic pressure dropped by a maximum of 30% at the 24th hour (23.1 +/- 5.1 to 16 +/- 5.4 mm Hg; p < 0.01). This decrease remained significant on day 7; the index cardiac was increased a maximum of 40% between the 18th and the 24th hour; p < 0.01). This increase was still significant on day 7 (2.35 +/- 0.44; p < 0.05; +22%). Finally, the decrease in systemic arterial resistance, which reached a maximum of 30% of the 24th hour, persisted on day 7 (-22%); 2076 +/- 451 to 1612 +/- 283 dynes/sec/cm5; p < 0.05). The norepinephrine level did not change significantly (4.5 +/- 1.2 nmol/l before infusion vs. 4.2 +/- 1.1 nmol/l on day 7). Infusion had to be stopped in one patient after 30 minutes because of prolonged severe hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to evaluate the efficacy and pharmacokinetics of enoximone administered as an intravenous bolus in 12 patients (mean age 62 years) with severe chronic congestive cardiac failure (Stage IV of the NYHA) due to ischemic (N = 6) or idiopathic (N = 6) cardiomyopathy. The haemodynamic parameters and plasma concentrations of enoximone and its metabolite were measured 15, 30, 60, 90, 120 minutes, 4 and 6 hours, after IV bolus of enoximone 1 mg/kg in 10 minutes. Enoximone increased the cardiac index by an average of 37 p. 100 (1.92 +/- 0.3 to 2.63 +/- 0.35 l/mn/m2; p less than 0.001); pulmonary artery diastolic pressures fell by 33 p. 100 (p less than 0.01). Systemic arterial resistances decreased by 23 p. 100 (p less than 0.05). No significant changes in heart rate or blood pressure were observed. The peak effect was recorded between the 15th and 30th minute. The pharmacokinetic study showed the half life of enoximone to be 2.2 +/- 0.78 hours, the area under the curve to be 2,818 +/- 953, the volume of distribution to be 69.6 +/- 24 l and the total clearance to be 22.8 +/- 8.5 l/hour. The half life of the metabolite was 4.45 +/- 1.05 hours. There was a significant correlation between the percentage increase in cardiac index and peak enoximone concentration (r = 0.91; p less than 0.001). In conclusion, an IV bolus of enoximone is an effective treatment for chronic cardiac failure. The haemodynamic response was related to the peak enoximone plasma concentration.

Cardiac failure is usually defined according to clinical and haemodynamic criteria at rest although these patients are mainly symptomatic on effort. Is it possible to substitute or associate a more "objective" method to the NYHA functional classification such as exercise stress testing? If so, is there a correlation between these two types of classification and resting haemodynamic data; have they any predictive value of the patient's exercise capacity? Twenty two patients with severe cardiac failure (Class III or IV of the NYHA), 18 men and 4 women with a mean age of 58 years, underwent a triangular exercise stress test on a bicycle ergometer to 80 p. 100 or more of their theoretical maximal heart rate. The ergometric parameters chosen for the study were the maximal oxygen consumption or its value when limited by symptoms, the maximal work with respect to weight, the total duration of exercise and the percentage increase in systolic blood pressure. The haemodynamic parameters chosen were pulmonary capillary pressure, systolic index, ejection fraction and the velocity of circumferential fibre shortening. No correlation was found between the NYHA functional class and exercise capacity. A dissociated correlation was observed between exercise capacity and resting haemodynamic data. The best correlation was between systolic index and exercise capacity (work performed corrected for body weight, r = 0.70, p less than 0.01; oxygen consumption, r = 0.60, p less than 0.01). After one month of treatment with a vasodilator (Prazosin) in 10 patients, the duration of exercise increased by 2.2 +/- 0.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this paper is to study the clinical and haemodynamic tolerance of intravenous diltiazem in a bolus dose of 10 mg followed by an infusion of 360 mg over 24 hours in 12 patients in the acute phase of myocardial infarction. We did not observe any significant modification in the heart rate or in the pulmonary artery diastolic pressure. The mean blood pressure decreased from 111.5 +/- 11.8 mmHg to 92.8 +/- 12.7 mmHg (p less than 0.001) after a 24 infusion. The cardiac index increased from 2.34 +/- 0.62 1 X min1 X m-2 to 3.05 +/- 0.95 1 X min-1 X m-2 (p less than 0.05) and the systemic vascular resistance decreased from 2 150 +/- 640 dyn. s.cm-5 to 1 403 +/- 308 dyn.s.cm-5 (p +/- 0.005). Three patients presented a rise in the pulmonary artery diastolic pressure of more than 30 mmHg and in one of these patients, the diltiazem had to be stopped. These three patients all had a high initial pulmonary capillary pressure (greater than 18 mmHg). The drug was well tolerated clinically. On electrocardiography, four patients presented conduction disorders, all of which regressed when the diltiazem was stopped (a 3rd degree atrioventricular block with narrow QRS complexes, a Luciani-Wenckebach type of 2nd degree atrioventricular block and two cases of 1st degree atrioventricular block. Overall, intravenous diltiazem was well tolerated in terms of clinical and haemodynamic parameters in these patients in the acute phase of a myocardial infarction, provided the left ventricular filling pressure was not excessively elevated.(ABSTRACT TRUNCATED AT 250 WORDS)

Reciprocal ST segment changes are frequent during acute inferior myocardial infarction, yet their significance remains controversial. In order to investigate the implications of these changes, the ECG obtained on admission for 83 patients with acute inferior myocardial infarction was compared with the clinical course and the results of angiographic and coronary arteriographic studies performed an average of 3 weeks after the onset of symptoms. Group 1 consisted of 59 patients with at least 1 mm of horizontal on downsloping ST segment depression in at least 1 of leads V1 to V4. Groups 2 consisted of 24 patients without precordial ST depression in this area. Group 1 patients were generally older than group 2 patients (59.6 +/- 6.4 versus 54 +/- 5.3 yr, P less than 0.01) had higher total creatine kinase (CK) levels and MB fractions (1835 +/- 940 versus 875 +/- 305, P less than 0.01, 269 +/- 102 versus 95 +/- 35 for MB fraction) and more complications during the hospital course (80% versus 38% P less than 0.01) and greater left ventricular dysfunction (ejection fraction 52.2 +/- 6% for group 1 versus 59.2 +/- 7% for group 2; cardiac index 2.75 +/- 0.41 min-1 m-2 for group 1 versus 3.25 +/- 0.31 min-1 m-2 for group 2 P less than 0.005). No difference was observed on biplane angiography as far as left ventricular wall kinesis was concerned.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this work is the evaluation of the hemodynamic effects during the 24 hours following a single administration of a new arterial vasodilator, cadralazine, in 12 patients whose mean age is 66 years and who present severe cardiac insufficiency. A clinical and hemodynamic examination was made before administration of the medicine in 3 doses at 12 hour intervals in order to check the stationary state of the patients, and then at 1 h, 2 h, 4 h, 6 h, 8 h, 12 h, 20 h and 24 h after 30 mg, and then 60 mg of cadralazine. We did not observe any significant change in cardiac frequency, nor in the systolic arterial pressure nor in the diastolic arterial pressure of the pulmonary artery, after either 30 mg or 60 mg. On the other hand, with 30 mg of cadralazine we observed a significant increase of the cardiac index, with a maximum between the 6th and 8th hour (1.58 +/- 0.51 l.min-1.m-2 before treatment to 2.66 +/- 0,75 l.min-1.m-2 8 hours after, p less than 0.001) and a fall of total systemic resistance which declined from 2,478 +/- 421 dyn.s-1.cm-5 before treatment to 1,449 +/- 369 dyn.s-1.cm-5, p less than 0.001, 8 hours after, as well as an increase in the power of the left ventricule (from 2.80 +/- 0.8 before treatment to 4.73 +/- 1.2 kg/min 8 hours after, p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this study was to evaluate the haemodynamic effects of slow release isosorbide dinitrate (IDN) 40 mg oral preparation over a 48 hour period in patients with acute myocardial infarction complicated by left ventricular failure. Fourteen patients (8 male, 6 female) were treated by repeat dose ISD (8 hourly) and the haemodynamic changes were recorded at 1 hr, 2 hrs, 6 hrs, 12 hrs, 24 hrs, and 48 hrs. After 48 hours treatment the heart rate was unchanged; mean arterial blood pressure fell from 109.5 +/- 5.6 mmHg to 93.5 +/- 6.2 mmHg (-15%) (p less than 0.01). Cardiac index rose from 2.4 +/- 0.57 1/min/m2 to 2.8 +/- 0.65 1/min/m2 (+16%) (NS); diastolic pulmonary artery pressure fell from 22.5 +/- 7.07 mmHg to 13.7 +/- 4.5 mmHg (-39%) (p less than 0.003); systolic pulmonary artery pressure fell from 40.5 +/- 12.2 mmHg to 28.6 +/- 11.6 mmHg (-30%) (NS). Systemic vascular resistance fell from 2 095.2 +/- 63 dynes/s/cm5 to 1 537 +/- 60 dynes/s/cm5 (-22.3%) (NS). Finally, total pulmonary resistance fell from 561.9 +/- 15 dynes/s/cm5 to 301.9 +/- 14.5 dynes/s/cm5 (-47%) (p less than 0.003). The most valuable effect was therefore the reduction in left ventricular filling pressures which was maximal after about 48 hours. Two groups of patients were identified according to the clinical outcome. The patients in Group I (11 cases) were improved by the fall in diastolic pulmonary artery pressure, the rise in cardiac index and the reduction of systemic valvular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

The prognostic value of right cardiac catheterization in the acute phase of myocardial infarction is presently well established. The objective of this study is to determine the best discriminating threshold of the pulmonary capillary pressure (PCP) on the one hand and the cardiac index on the other hand. 96 patients presenting an acute myocardial infarction were entered in the study. Six thresholds for each parameter were studied. The following results were obtained: there are important clinical and hemodynamic discrepancies, especially for severe cases. The cardiac index (CI) has a better prognostic value than the pulmonary capillary pressure. The threshold greater than 18 mmHg for PCP and less than 2.2 l/min for the cardiac index, proves to be the most discriminating (better sensitivity with better specificity: sensitivity 60 p. cent with specificity at 81 p. cent for PCP; sensitivity at 73 p. cent with specificity at 78 p. cent for CI). A combined analysis of the two parameters, associated to their best discriminating threshold enables to identify a class of high-risk patients presenting approximately an 80 p. cent mortality in a hospital environment. In spite of the development of non-invasive methods to evaluate the prognosis in the acute phase of myocardial infarction, the hemodynamic exploration remains the leading method for its evaluation.

Abstract: Objectives: To characterize and compare patients with disproportionate PH versus patients with primary pulmonary arterial hypertension (PAH). Methods: All patients referred to our cardiology unit for echocardiography from November 2006 to May 2008 and who have been followed by our pneumologist were screened for severe PH (i.e mean arterial pulmonary pressure>35–40mmHg at rest). Patients were excluded if a factor that could influence pulmonary hemodynamics was present. We investigated these patients by pulmonary function tests, echocardiography and right heart catheterisation. Results: We reported 16 cases of severe PH in stable patients (n =8, chronic obstructive pulmonary disease-emphysema) and 13 patients with PAH. Our findings suggest that the patients with disproportionate PH had right heart dysfunction similar to that observed in PAH. But their outcomes were more severe. It seemed that specific vasodilatator therapy was not efficient. [Copyright &y& Elsevier]