[Impact of preoperative 64-row multislice computed tomography for congenital aortic stenosis; report of a case].

A 63-year-old woman was diagnosed as having severe aortic stenosis (AS) with 98 mmHg peak pressure gradient detected by echocardiography. Since, preoperative enhanced 64-row multislice computed tomography (MSCT) showed bicuspid aortic valve with only 2 sinuses of Valsalva, congenital aortic stenosis was suspected. The left and right coronary arteries originated from respective sinus of Valsalva, and severely thickened cusps of aortic valve were detected clearly by preoperative 64-row MSCT. Aortic valve replacement with a 21 mm ATS mechanical bileaflet prosthesis was performed without aortic annulus enlargement. The postoperative course was uneventful and postoperative 64-row MSCT indicated good performance of the ATS valve. Preoperative 64-row MSCT could be useful to detect complex aortic valve disease in detail. Moreover. 64-row MSCT might be a reliable tool to evaluate valvular heart disease.

A new procedure for chronic atrial fibrillation: bilateral appendage-preserving maze procedure.

BACKGROUND: Atrial transport and atrial natriuretic peptide secretion is severely reduced from normal after the maze III procedure. To improve these factors, we developed a bilateral appendage-preserving maze procedure (BAP-maze). METHODS: Forty-six patients with chronic atrial fibrillation who underwent the BAP-maze procedure were compared with 40 patients who underwent the maze III procedure. The ratio of the peak velocity of the A and E waves of transmitral flow (transthoracic pulsed Doppler echocardiography), the left atrial appendage ejection fraction (transesophageal echocardiography), and the atrial natriuretic peptide secretory reserve during treadmill exercise test were measured at 6 months postoperatively. RESULTS: Sinus rhythm was restored in 44 patients (95.7%) by the BAP-maze procedure and in 39 patients (97.5%) by the maze III procedure. The ratio of the peak velocity of the A and E waves was 0.52 +/- 0.22 in the BAP-maze group and 0.25 +/- 0.19 in the maze III group (p < 0.0001). The left atrial appendage ejection fraction was 44.7% +/- 11.5%, and the atrial natriuretic peptide secretory reserve was greater in the BAP maze group (p = 0.037). CONCLUSIONS: The BAP-maze procedure improved atrial transport and atrial natriuretic peptide secretion as well as simplifying the maze operation, without decreasing its effectiveness against atrial fibrillation.

Early and late outcomes after reoperation for prosthetic valve endocarditis.

OBJECTIVE: Prosthetic valve endocarditis remains a challenging complication after heart valve replacement. To identify predictive risk factors, we have reviewed 30 patients who underwent surgery for prosthetic valve endocarditis between March 1986 and May 1999. METHODS: There were 15 men and 15 women (mean age 51 years). Prosthetic valve endocarditis was classified as early (< or = 1 year after operation) in 10 cases, and as late in the other 20 cases. The most common indication for surgery was moderate to severe congestive heart failure due to prosthetic valve dysfunction in 21 (70%) patients. The average follow-up period was 6.5 years, with a range of 0.3 to 14.1 years. RESULTS: The most common microorganism was Staphylococcus epidermidis in both patients with early (50%) and late prosthetic valve endocarditis (25%). The in-hospital mortality was 13.3% (4/30). There were six late deaths. The actuarial survival at 5 years was 78% and 66% at 10 years. An early onset of prosthetic valve endocarditis was the only significant determinant of both in-hospital mortality (p = 0.005) and overall mortality (p = 0.021). Emergency surgery had a statistically significant relationship with in-hospital mortality (p = 0.045). No significant influence on mortality after reoperation for prosthetic valve endocarditis was found in age, sex, valve position, antecedent native valve endocarditis, or in the type of pathological findings (ring abscess, valve dehiscence, and vegetation). CONCLUSION: Early onset of prosthetic valve endocarditis and emergency surgery were important risk factors for mortality due to prosthetic valve endocarditis.

Mitral insufficiency associated with primary antiphospholipid syndrome and chronic renal failure.

We report a case of 52-year-old woman with primary antiphospholipid syndrome who developed mitral insufficiency and chronic renal failure. Continuous ambulatory peritoneal dialysis was started preoperatively due to thrombocytopenia that was aggravated by hemodialysis. Mitral annuloplasty was performed since the mitral valve was not severely damaged. Her postoperative hemodynamics were stable, and anticoagulant therapy was controlled easily. She recovered from severe thrombocytopenia while on continuous ambulatory peritoneal dialysis. Valvular heart disease is a well known feature of primary antiphospholipid syndrome, and there have been several reports about valve replacement in patients who had antiphospholipid syndrome with or without systemic lupus erythematosus. However, valve repair has been reported in only a few such patients. We believe that valve repair is better than valve replacement in patients with antiphospholipid syndrome because of its hypercoagulable tendency. In addition, it seems that continuous ambulatory peritoneal dialysis is a suitable method for the perioperative management of patients with antiphospholipid syndrome who suffer from chronic renal failure as well as thrombocytopenia, and require cardiac surgery under cardiopulmonary bypass.

Secondary mitral valve replacement in antiphospholipid syndrome and chronic renal failure.

A 48-year-old woman admitted with progressive dyspnea had previously been diagnosed with systemic lupus erythematosus, antiphospholipid syndrome, and chronic renal failure, and had undergone mitral valve replacement with a Carpentier-Edwards pericardial bioprosthesis for mitral insufficiency 9 years before. She suffered a cerebral infarction 5 years earlier, despite appropriate anticoagulant therapy. On admission, echocardiography showed severe bioprosthetic stenosis. Repeat mitral valve replacement was conducted using a Mosaic bioprosthesis. On postoperative day 2, when heparinization was commenced, she suddenly had an epileptic fit. She also developed ischemic necrosis of the fingers and toes, considered secondary to microthrombosis. Aspirin was administered and heparin replaced by warfarin sodium. Necrosis gradually disappeared, and she was discharged 3 months after surgery. The original bioprosthesis showed degenerative changes with significant thrombus formation on cusps, thought to be mainly due to her hypercoagulable state. Considering the thrombophilic tendency in patients with antiphospholipid syndrome, strict management of anticoagulant therapy is required.

Intravenously-injected naloxone reverses the decrease in renal sympathetic nerve activity seen during hypotensive hemorrhage in conscious rabbits by acting through central mechanisms.

The response of renal sympathetic nerve activity (RNA) to hemorrhage was examined in chronically-instrumented conscious rabbits. Hemorrhage was induced at a rate of 5 ml/kg per min until the mean arterial pressure fell below 40 mmHg. The mean arterial pressure then remained at around 80 mmHg until 10 ml/kg of hemorrhage (normotensive hemorrhage) before falling to below the pre-hemorrhagic control level (hypotensive hemorrhage). The RNA response showed a biphasic pattern, i.e., it increased during normotensive hemorrhage, then fell below the control level during hypotensive hemorrhage. To examine the mechanism involved in this decrease in RNA, naloxone (7.5 mumol/kg), an opioidergic receptor antagonist, was intravenously injected 1 min after the end of hemorrhage. Intravenous injection of naloxone caused an increase in mean arterial pressure and RNA to the level seen during normotensive hemorrhage. These results indicate that the decrease in RNA induced by hypotensive hemorrhage is mediated by opioidergic receptors. To determine whether the effects of naloxone are mediated via central or peripheral opioidergic receptors, naloxone was replaced by an equimolar solution of methylnaloxone, a form unable to cross the blood-brain barrier. Neither the mean arterial pressure nor RNA was significantly altered by administration of methyl naloxone. These results suggest that the effects of naloxone on both the RNA and the mean arterial pressure are mediated via central opioidergic receptors, i.e., the sympathoinhibition induced by hypotensive hemorrhage is mediated via the stimulation of central opioidergic receptors.

Role of endogenous opioids and central opioid receptors in cerebral cortical blood flow autoregulation.

To examine the role of endogenous opioids in autoregulatory maintenance of cerebral cortical blood flow (CoBF), CoBF was measured continuously by laser-Doppler flowmetry during changes in arterial pressure. Experiments were conducted on pentobarbital sodium-anesthetized adult mongrel dogs. Mean arterial pressure (MAP) was decreased or increased by inflating a perivascular occluder placed around the inferior vena cava or the thoracic descending aorta, respectively. To exclude the influence of the baroreceptor reflex on the autoregulatory maintenance of CoBF, all experiments were conducted on dogs with bilateral carotid sinus denervation plus vagotomy. CoBF was well maintained within its normal range despite large changes in MAP. Intravenous injection of naloxone (2.5 mumol/kg), an opioid receptor antagonist, significantly impaired the autoregulatory maintenance of CoBF during the decrease in MAP. On the other hand, intravenous injection of methyl naloxone (2.5 mumol/kg), which does not cross the blood-brain barrier, did not exert any significant effect on the MAP-CoBF relationship. Furthermore, intracerebroventricular injection of a smaller dose of naloxone (2.5 nmol/kg) significantly impaired the autoregulatory maintenance of CoBF during the decrease in MAP, as the larger dose of intravenous naloxone (2.5 mumol/kg) did. On the other hand, intravenous injection of the smaller dose of naloxone did not exert any significant effect on the MAP-CoBF relationship. These findings suggest that endogenous opioids and central opioid receptors may be partly involved in the CoBF autoregulatory mechanism. The endogenous opioids may modulate the autoregulatory vasodilation of the cerebral cortex during the decrease in MAP.