[Uncommon cause of mitral insufficiency: pacemaker lead malpositioning in the left ventricle. Case report]. / Cause inhabituelle d'insuffisance mitrale: implantation involontaire d'une sonde de stimulation endocavitaire dans le ventricule gauche. A propos d'un cas.

Cardiac pacemakers' insertions may be associated with different types of complications such as lead's malposition. The authors report the observation of lead's malposition in the left ventricular chamber through the interatrial septum. This malposition is potentially dangerous because of the potent risk factor for stroke and thromboembolism that the patient might run. The diagnosis of this malposition can be done by surface electrocardiogram and thorax X-ray. However, we do insist on the importance of echocardiography and furthermore of transesophageal echocardiography which can lead to a much better choice in the treatment.

Ruptured aortic dissection into the left atrium which presented as congestive heart failure and was diagnosed by transoesophageal echocardiography.

A 72 year old man was admitted with severe dyspnoea. Ten days before he had had intense thoracic pain with loss of consciousness that was followed by increased dyspnoea. A continuous murmur was heard in the precordial and the left infrascapular regions. Lung auscultation showed stasis over the lower half of both lungs. Transthoracic echocardiography showed a bicuspid aortic valve and a dissection of the proximal aorta, which was considerably enlarged. Transoesophageal echocardiography confirmed dissection of the proximal aorta and showed a communication from the false lumen of the aortic dissection to the left atrium; and colour flow Doppler showed a continuous shunt to the left atrium. After transoesophageal echocardiography the patient had emergency surgical repair, which was successful. He had no complications in the post-operative period.

Transesophageal echocardiography of right atrial metastasis of a hepatocellular carcinoma.

Antemortem diagnosis of cardiac metastases of a hepatocellular carcinoma is rarely observed. In a 52-year-old female patient with a history of posthepatitic cirrhosis and partial hepatectomy, transthoracic echocardiography brought to light a mass in the right atrium. After location and characterization of the tumor by transesophageal echocardiography, a transvenous biopsy confirmed the diagnosis of metastasis of a hepatocellular carcinoma.

Cardiovascular protection by estrogen: a hemodynamic mechanism?

Cardiovascular risk is higher in men than in women, and also more prevalent in postmenopausal than in premenopausal women, especially if not treated by estrogens. These differences may be due, in part, to a cardioprotective action of sex hormones, mainly estrogens. However, only a limited part of this protection may be attributed to metabolic modifications induced by replacement therapy with estrogen. Therefore, it remains to be determined which other cardioprotective mechanisms influenced by sex steroids might be involved. It has been demonstrated that the menopause is associated with an increase in uterine arterial pulsatility index, reflecting increased peripheral resistance, while the administration of estrogens has an opposite effect at this level. In Doppler studies, estrogen replacement therapy was also associated with an increase in stroke volume and flow acceleration in the aorta. This suggests a positive inotropic effect of estrogens. Using technetium scanning, it was found that women at an early phase of menopause have a stronger myocardial contractility than women of a similar age whose menopause is of longer duration. These effects of estrogens on hemodynamic characteristics might be controlled by vasoregulatory hormones such as endothelin(s) or endothelial-derived relaxing factor (EDRF), now identified as nitric oxide (NO). Indeed, sex-associated differences in endothelin have been observed. Such are some of the mechanisms by which estrogen administration might effect a cardiovascular protection. At the present time, however, conclusive data are not available.

Electrophysiologic effects of intravenous xamoterol in patients with sinus node dysfunction.

The electrophysiologic effects of xamoterol were studied in ten patients with electrophysiologic evidence of sinus node dysfunction. A significant shortening of mean sinus cycle length, maximal corrected sinus-node recovery time, and the mean of the three longest corrected sinus-node recovery times was observed after intravenous administration of 0.1 mg/kg of xamoterol. The atrioventricular (AV) conduction time and the effective and functional refractory periods of the AV node were shortened as the effective refractory period of the atrium. These effects suggest that xamoterol could be tried safely for the treatment of patients with moderate symptoms due to sinus-node disease.

Pimobendane (UD-CG 115 BS) in chronic congestive heart failure. Short-term and one-month effects of a new inotropic vasodilating agent.

We studied the effects of oral administration of pimobendane on hemodynamics, blood gas levels, the renin-angiotensin system, and plasma catecholamines in 11 patients who were affected by severe chronic congestive heart failure. Following the administration of 5 mg, the cardiac index increased from 2.0 +/- 0.2 to 2.5 +/- 0.2 L/min/m2 (p less than 0.01), and the pulmonary wedge pressure decreased from 28 +/- 3 to 17 +/- 4 mm Hg (p less than 0.01). The maximal changes were noted five hours after intake of the drug. In spite of a significant decrease in arterial oxygen pressure (PaO2) (from 81 +/- 4 to 67 +/- 5 mm Hg; p less than 0.05), a significant increase in the oxygen delivery index was seen (from 322 +/- 32 to 436 +/- 38 ml/min/m2; p less than 0.01). The patients who were submitted to long-term treatment (5 mg twice daily) and who were reassessed after at least one month exhibited an improved cardiac index from 1.9 +/- 0.2 to 2.5 +/- 0.1 L/min/m2 (p less than 0.01), as well as a decreased pulmonary wedge pressure from 26 +/- 2 to 14 +/- 4 mm Hg (p less than 0.01). The norepinephrine levels were significantly reduced after one month (from 1,496 +/- 185 to 678 +/- 95 pg/ml; p less than 0.01), whereas the plasma renin activity was not. One patient died suddenly during the one-month follow-up period. With the exception of one case, which was also treated with heparin, a transient cutaneous rash and a drop in the level of blood platelets were observed, pimobendane was well tolerated. This new inotropic and vasodilating drug thus seems to have promise for the treatment of chronic congestive heart failure.

Pimobendane (UD-CG 115 BS) in the treatment of severe congestive heart failure. An acute haemodynamic cross-over and double-blind study with two different doses.

1. We compared the effects of two doses (5 and 10 mg) of oral pimobendane (UD-CG 115) on haemodynamics in eight patients suffering from chronic congestive heart failure. The two doses were given according to a randomized cross-over double-blind protocol; haemodynamics and plasma levels of pimobendane and its main metabolite UD-CG 212, were determined 1, 2, 3, 5, 7, 9, 11 and 12 h after each dose. 2. Both doses significantly improved the left and right ventricular functions of these patients, with a peak action 3 h after drug intake and long duration (more than 12 h). A significant dose-effect relationship was observed only for pulmonary wedge pressure and right atrial pressure. Significant correlations were found between UD-CG 212 plasma levels and cardiac index (r = 0.54, P less than 0.05), and pulmonary wedge pressure (r = 0.74, P less than 0.001); no correlation was found between these haemodynamic variables and pimobendane plasma levels. 3. One patient developed a transient drop in blood platelets together with a cutaneous rash, while three others had a transient and mild decrease of thrombocytes. 4. In conclusion, pimobendane improved right and left ventricular functions in severe heart failure. Both doses (5 and 10 mg) were effective. The higher dose induced marked improvement of the haemodynamic variables but the difference between doses was only significant for right atrial and pulmonary wedge pressures.

Central inhibition of sympathetic overdrive by clonidine in acute myocardial infarction with systolic hypertension. Haemodynamic study.

Intravenous clonidine was used to treat systolic hypertension (systolic blood pressure greater than 160 mm Hg) in 15 patients with acute myocardial infarction and documented sympathetic overactivity (high plasma norepinephrine). Its effects on haemodynamics and blood gases were studied. After one hour, clonidine significantly reduced the systolic (195 +/- 7 to 137 +/- 7 mm Hg, p less than 0.01) and diastolic (81 +/- 4 to 60 +/- 3 mm Hg, p less than 0.01) blood pressures as well as the systemic vascular resistance (26 +/- 2 to 20 +/- 1 IU, p less than 0.01). The cardiac index was reduced from 2.8 +/- 0.2 to 2.4 +/- 0.2 l/min X m2, p less than 0.01. This change was related to a reduction of the heart rate (92 +/- 4 to 81 +/- 4 beats/min, p less than 0.01) as the stroke index was unchanged. Pulmonary wedge pressure (15 +/- 3 to 10 +/- 2 mm Hg, p less than 0.01) and rate pressure product (18.034 +/- 1.159 to 11.274 +/- 917 mm Hg, beats/min, p less than 0.01) were also significantly decreased. The arterial oxygen tension did not change significantly but there was a significant drop in the mixed venous oxygen saturation (63 +/- 2 to 61 +/- 2%, p less than 0.02) and oxygen transport (433 +/- 41 to 409 +/- 36, p less than 0.01). Clonidine is thus able to normalize blood pressure in acute myocardial infarction; this is accompanied by a reduction in myocardial oxygen requirements and pulmonary wedge pressure. Oxygen transport to the tissues, however, may be decreased.

[Hemodynamic repercussions and clinical tolerance of 6 class I anti-arrhythmia agents in acute myocardial infarction]. / Répercussions hémodynamiques et tolérance clinique de six agents antiarythmiques de la classe I dans l'infarctus aigu du myocarde.

Clinical safety and hemodynamic repercussions were studied after administration of six class I antiarrhythmics (xylocaine, ajmaline, mexiletine, lorcainide, indecainide and tocainide) to patients presenting acute myocardial infarction without complications. The hemodynamic parameters monitored generally followed the same trends. A significant decrease of more than 10 per cent of the initial value was seen in systolic blood flow after injection of lorcainide, indecainide and tocainide. Peripheral vascular resistance increased moderately. Pulmonary capillary pressure increased by more than 40 per cent of the starting value after administration of mexiletine, indecainide and tocainide (significant increase in case of mexiletine). These changes in patients presenting infarction without complications are not of clinical importance. There were, however, two very severe cases of hemodynamic reaction after administration of mexiletine. Other signs of intolerance were seen, but they were of minor importance and administration of the drugs was not interrupted. Xylocaine and ajmaline produced the smallest depression of left ventricular functional activity in these patients.

A comparison of the effects of combined or separate alpha- and beta-blockade in the treatment of hypertension in the acute stage of myocardial infarction.

We have assessed the benefit of separate or combined alpha- and beta-receptor blockade in the treatment of 33 patients suffering from acute (less than 48 hr) myocardial infarction complicated by sustained (greater than 6 hr) systolic hypertension (systolic blood pressure greater than 150 mm Hg). Eight patients have been treated with metoprolol, 7 with phentolamine and 18 with labetalol. We evaluated the effects of these drugs on hemodynamics and arterial and mixed venous blood gases. The patients were divided into two groups on the basis of the pulmonary wedge pressure. The first group had a pressure greater than 15 mm Hg. It included 9 patients treated with labetalol (1.8 mg/min for 1 hr) and 7 others with phentolamine (0.6 mg/min for 1 hr). The wedge pressure in the second group was less than 13 mm Hg. Nine patients in this group had been treated with labetalol (2.1 mg/min for 1 hr) and 8 others with metoprolol (0.2 mg/kg in 15 min). Labetalol normalized the blood pressure in both groups within 1 hr as did phentolamine. Metoprolol did not significantly reduce either the systolic or the diastolic pressures. The high wedge pressures in the first group were reduced by both labetalol and phentolamine. The cardiac index was increased following phentolamine administration while it was reduced by labetalol. In the group with low wedge pressure, labetalol and metoprolol induced a slight but significant reduction in cardiac index but the pulmonary wedge pressures were significantly increased for metoprolol only. The rate-pressure product was very significantly decreased by labetalol and metoprolol but not by phentolamine. The emergency treatment of systemic hypertension occurring in the setting of acute myocardial infarction would thus appear to be best achieved by combined alpha- and beta-blockade rather than with either pure alpha- or pure beta-blockade. Phentolamine, however, would be a good drug in the presence of a reduced cardiac index.

Blood gas and hemodynamic changes induced by the treatment of pulmonary congestion with vasodilators in the acute phase of myocardial infarction.

The effects of vasodilators on hemodynamics and blood gases was assessed in 31 patients suffering from acute myocardial infarction (AMI) who had clinical signs of left ventricular failure with high pulmonary wedge pressure (PWP greater than 15 mm Hg). Molsidomine (n = 10), phentolamine (n = 12) and sulmazol (n = 9) were administered intravenously to decrease the PWP by 20%. Molsidomine significantly decreased PWP after one hour with a mild increase in cardiac index (CI) inducing a slight decrease in paO2 (64 to 59 mm Hg, P less than 0.1) with no change in p-vO2. Phentolamine and Sulmazol significantly increased the CI and decreased the PWP, with a substantial increase in the pv-O2 (28 to 32 mm Hg, P less than 0.005 and 28 to 31 mm Hg, P less than 0.001) and no significant change in the paO2 (60 to 65 mm Hg, P less than 0.1 and 68 to 69 mm Hg, NS). None of these drugs significantly changes the pulmonary vascular resistance (PVR) which would explain the lack of any significant change in paO2. The treatment of pulmonary congestion in AMI by either pure venous (molsidomine) or arteriolar and venous (phentolamine and sulmazol) vasodilators does not worsen obviously pre-existant hypoxemia.

Effects of molsidomine on hemodynamics and blood gases in acute myocardial infarction with left heart failure.

We studied the effects of molsidomine on hemodynamic properties and blood gas levels in eight patients with acute myocardial infarction and left heart failure. One hour after an 8 mg intravenous bolus injection, pulmonary wedge pressure and right atrial pressure decreased, respectively, from 30 +/- 9 to 23 +/- 12 mm Hg (p less than 0.01) and from 10.4 +/- 3.6 to 7.8 +/- 4.0 mm Hg (p less than 0.05) without significant changes in heart rate, cardiac index, or systemic blood pressure. There was a mild decrease in arterial oxygen tension (from 61 +/- 15 to 56 +/- 6 mm Hg), but it was not significant. The drug induced no adverse effects. Intravenous bolus injection of molsidomine rapidly relieves pulmonary congestion in patients with acute myocardial infarction.