Clinical, echocardiographic, and hemodynamic characteristics of rheumatic mitral valve stenosis and atrial fibrillation

Chronic atrial fibrillation (AF) is associated with an increased frequency of embolic events and negative impact on cardiac function, and therefore, an increased morbidity and mortality risk in patients with rheumatic mitral valve stenosis (RMS). In the present study, the clinical, 2-D and Doppler echocardiographic, and left-and right-heart hemodynamic data were evaluated for 92 patients (68 women) with RMS and AF and compared with data from 118 patients (88 women) with RMS with sinus rhythm. The clinical, echocardiographic, and hemodynamic evaluations were performed within 1 to 7 days of each other. Patients with AF were older (45.7+/-13.4 vs 38.6+/-12.0 years, p < 0.01) and had a longer symptomatic period (108.2+/-117.9 vs 50.6+/-53.1 months, p < 0.01) compared with those with sinus rhythm. Most of the patients with AF were in NYHA functional capacity 3-4 (74% vs 19%), whereas most of the patients with sinus rhythm were in NYHA functional capacity 2. Patients with AF had a higher mitral valve score based on morphologic features ranging from 4 to 16 depending on the severity of disease (8.3+/-2.1 vs 6.5+/-1.9, p < 0.01) and greater left ventricular end-diastolic diameter (LVEDD) (52.3+/-8.7 vs 47.7+/-8.7 mm, p < 0.02), and end-systolic diameter (LVESD) (34.4+/-7.5 vs 30.9+/-7.5 mm, p < 0.01). Organic tricuspid valve involvement was diagnosed more frequently in patients with AF (61% vs 32%, p < 0.01). Mild mitral regurgitation was also more frequent in patients with AF (71%vs 51%, p < 0.03). The mitral valve area was similar in patients with and without AF (1.30+/-0.39 vs 1.39+/-0.41 cm2, p > 0.05). Mean diastolic mitral valve gradient and pulmonary artery pressure did not differ in patients with and without AF. Right atrial pressures were higher in patients with AF (7.6+/-3.3 vs 6.3+/-1.9 mm Hg, p < 0.02). The authors suggest that (1) AF occurred in older patients, who had a longer disease process and more serious symptoms; (2) hemodynamic derangements (mitral valve gradient, pulmonary artery pressure) did not differ in patients with and without AF; (3) greater mitral valve score, more tricuspid valve involvement, higher LVEDD, which are suggestive of greater rheumatic activity process were more frequently seen in patients with AF than in those without AF. These findings support the opinion that AF is a marker of widespread rheumatic damage in patients with RMS.     

Effect of cooled hyperbaric bupivacaine on unilateral spinal anesthesia success rate and hemodynamic complications in inguinal hernia surgery

Purpose

We hypothesized that cooling hyperbaric bupivacaine from 23 to 5 °C may limit the intrathecal spread of bupivacaine and therefore increase the success rate of unilateral spinal anesthesia and decrease the rate of hemodynamic complications.

Methods

A hundred patients scheduled for elective unilateral inguinal hernia surgery were randomly allocated to receive 1.8 ml of 0.5 % hyperbaric bupivacaine intrathecally at either 5 °C (group I, n = 50) or at 23 °C (group II, n = 50). Following spinal block at the L2-3 interspace, the lateral decubitus position was maintained for 15 min. Unilateral spinal anesthesia was assessed and confirmed at 15 and 30 min. The levels of sensory and motor block on the operative side were evaluated until complete resolution.

Results

The rate of unilateral spinal anesthesia at 15 and 30 min was significantly higher in group I (p = 0.015 and 0.028, respectively). Hypotensive events and bradycardia were significantly rarer in group I (p = 0.014 and 0.037, respectively). The density and viscosity of the solution at 5 °C was significantly higher than at 23 °C (p < 0.0001). Compared with group II, sensory block peaked later in group I (17.4 vs 12.6 min) and at a lower level (T9 vs T7), and two-segment regression of sensory block (76.4 vs 84.3 min) and motor block recovery was shorter (157.6 vs 193.4 min) (p < 0.0001).

Conclusions

Cooling of hyperbaric bupivacaine to 5 °C increased the density and viscosity of the solution and the success rate of unilateral spinal anesthesia, and decreased the hemodynamic complication rate.

     

The effect of pentoxifylline on the healing of intestinal anastomosis in rats with experimental obstructive jaundice

The aims of this study were (1) to investigate the effect of experimental obstructive jaundice on the healing of intestinal anastomosis, and (2) to investigate the effect of pentoxifylline on the healing of intestinal anastomosis in rats with obstructive jaundice. Obstructive jaundice was induced in rats by the ligation and division of the common bile duct. Four days after this operation, either pentoxifylline or isotonic saline solution was administered intraperitoneally to these jaundiced rats and controls, and then intestinal anastomosis was performed. The concentrations of serum tumor necrosis factor α (TNF-α) and serum triglyceride of jaundiced and nonjaundiced rats were measured, and the quality of healing was evaluated by measuring the bursting preasure and hydroxyproline content of the anastomoses on the fifth and tenth days of anastomotic healing. Obstructive jaundice resulted in an impaired wound healing of the intestinal anastomosis in the rats. The administration of pentoxifylline to the jaundiced rats resulted in better anastomotic wound healing. The beneficial effects of pentoxifylline on anastomotic healing in rats with obstructive jaundice was attributed to its inhibitor effect on the endotoxin-induced TNF-α release from macrophages and monocytes, and the stabilizing effect on the neutrophils. Received: March 29, 1999 / Accepted: March 24, 2000     

Lacrimo-auriculo-dento-digital syndrome with QT prolongation

We present a case of a young boy in whom lacrimo-auriculo-dental-digital (LADD) syndrome with QT prolongation was detected. According to Bazett's formula, corrected QT was 504 ms. There were no published data about LADD syndrome with QT prolongation. This is the first case concerning LADD syndrome associated with QT prolongation. It is known that deafness and QT prolongation occur in potassium channel dysfunction. QT prolongation and deafness may be associated with potassium channel dysfunction in patients with LADD syndrome. As a result QT prolongation may be a new component of the LADD syndrome.     

Aortic valve aneurysm: a novel cardiac manifestation of rheumatoid arthritis?

This report describes a 51-year-old man with rheumatoid arthritis, coronary artery disease, left ventricular failure, and saccular aneurysm of the left coronary cusp of the aortic valve. Rheumatoid arthritis can involve the heart in several ways; however, aortic valve aneurysm in rheumatoid arthritis has not been reported before. Absence of vegetation, lack of a history of infective endocarditis, and the preservation of aortic valve function suggested that this saccular aneurysm was not a result of infective endocarditis. An intimal flap, which strongly suggests aortic dissection, was not observed. To our knowledge, this may be a novel cardiac manifestation of rheumatoid arthritis, and this is the first published report.     

Cardiac autonomic function evaluated by the heart rate turbulence method was not changed in obese patients without co-morbidities

Obese subjects are more prone to sudden deaths and arrhythmias than non-obese subjects. Heart rate turbulence (HRT) impairment reflects cardiac autonomic dysfunction, in particular impaired baroreflex sensitivity and reduced parasympathetic activity. Our aim was to evaluate the cardiac autonomic function in obesity by the HRT method. Ninety obese subjects and 112 healthy subjects were included in the study. Twenty-four hours ambulatory electrocardiograms were recorded and Holter recordings were analyzed. HRT parameters, turbulence onset (TO) and turbulence slope (TS), were calculated with HRT View Version 0.60-0.1 software program. HRT were calculated in 43 obese and 43 control subjects who had at least one ventricular premature beat in their Holter recordings. We excluded 47 obese patients and 69 control subjects who showed no ventricular premature beats in their Holter recordings from the statistical analysis. There were no significant differences in TO and TS between obese and control subjects (TO obese: -1.6 +/- 2.2%, TO control: -2.1 +/- 2.6%, p>0.05; TS obese: 8.2 +/- 5.2, TS control: 10.1 +/- 6.7, p>0.05, respectively). HRT parameters seem to be normal in obese patients without comorbidities.     

Comparison of the effects of ipratropium bromide and salbutamol on autonomic heart rate control.

AIMS: B2-agonists and anticholinergic drugs may alter cardiac autonomic modulation. The aim of this study was to investigate the effects of inhaled salbutamol and ipratropium bromide on heart rate variability (HRV). METHODS AND RESULTS: A randomized, double-blind, crossover design study was conducted on 13 healthy volunteers. Salbutamol, ipratropium or placebo was administered in three different testing sessions. Time domain parameters; mean R-R interval (mean-RR), the standard deviation of R-R interval (SDNN) and the root mean square of successive R-R interval differences (RMSSD) and power spectral analysis of HRV were assessed in the supine position and during handgrip exercise before and after taking each drug. In time domain analyses, ipratropium administration resulted in a reduced mean-RR, SDNN and RMSSD during handgrip exercise compared with baseline values (775 +/- 30 ms vs. 748 +/- 21 ms, P < 0.05; 57 +/- 5 ms vs. 50 +/- 5 ms, P < 0.05; 30 +/- 2 ms vs. 26 +/- 2 ms, P < 0.01, respectively). This effect was not detected with salbutamol or placebo administration. In frequency domain analyses, salbutamol but not ipratropium and placebo inhalation increased high frequency power/total power during handgrip exercise compared with baseline (0.09 +/- 0.02 vs. 0.12 +/- 0.02, P < 0.05). CONCLUSION: Ipratropium inhalation may alter autonomic control of the heart rate in therapeutic doses during mild sympathetic stimulation in healthy subjects, while salbutamol does not show these effects.     

Acute myocardial infarction associated with amitriptyline overdose

Tricyclic antidepressant overdose is known to cause cardiopulmonary and central nervous system complications. As with other cardiovascular complications, amitriptyline toxicity may cause acute myocardial infarction. This paper reports the case of a young female with acute myocardial infarction as a novel consequence of tricyclic antidepressant overdose.