Assessment of autonomic dysfunction and anxiety levels in patients with mitral valve prolapse.

OBJECTIVES: This study aimed to assess autonomic dysfunction parameters and anxiety levels in patients with mitral valve prolapse (MVP). STUDY DESIGN: We evaluated 33 patients (mean age 25+/-5 years) with MVP and 14 healthy subjects (mean age 25+/-4 years). The patients were divided into two groups according to the presence (anatomical MVP, n=11) or absence (MVP syndrome, n=22) of abnormal leaflet thickening (>5 mm). Spielberger's Situational Anxiety Scale (SSAS) and Continuous Anxiety Scale (SCAS) were administered to all the subjects, and heart rates (HR) and arterial blood pressures (BP) were measured in the supine and standing positions. RESULTS: Mid-systolic click and late systolic murmur were significantly more frequent in patients with anatomical MVP, while nonspecific symptoms such as dyspnea, vertigo, and atypical chest pain were more frequent in patients with MVP syndrome (p<0.05). Mitral insufficiency (mild) was significantly more frequent in patients with anatomical MVP (72.7% vs. 22.7%; p<0.009). Patients with MVP syndrome had significantly higher SSAS and SCAS scores (41.0+/-15.6 and 38.5+/-15.5) compared to patients with anatomical MVP (15.8+/-7.5 and 17.0+/-9.1) and controls (14.9+/-7.4 and 16.9+/-8.7, respectively; for both p<0.001). Orthostatic differences in BP and HR were significantly greater in patients with MVP syndrome than those having anatomical MVP (p<0.001 and p=0.032, respectively). Orthostatic HR differences showed a significant correlation with SSAS in both MVP groups (r=0.536, p=0.001) and a significant correlation with SCAS in patients with MVP syndrome (r=0.523, p=0.002). There was an inverse correlation between orthostatic BP differences and anxiety parameters in all MVP patients (r=-0.391, p=0.025 for SSAS, and r=-0.320, p=0.048 for SCAS). CONCLUSION: Our data suggest that patients with MVP syndrome have increased autonomic dysfunction and anxiety scores compared to patients with anatomical MVP.

Treatment of Brucella endocarditis: our surgical experience with 6 patients.

BACKGROUND: Endocarditis is a rare but life-threatening complication of brucellosis. Its mortality rate has recently been reduced with the use of combined medical and surgical treatment. METHODS: Between March 2002 and April 2004, 6 patients with Brucella endocarditis underwent surgery at the Siyami Ersek Cardiovascular Center in Istanbul, Turkey. The diagnosis of Brucellosis was based on the presence of clinical signs and symptoms compatible with brucellosis, serology and/or a positive blood culture. All patients with suspected Brucella endocarditis were studied by echocardiography. The diagnosis of Brucella endocarditis was made in accordance with Duke's criteria. RESULTS: The most commonly affected valve was the aortic valve (4 patients). Four patients had prosthetic valves because of a previous history of rheumatic fever. In 5 patients, elective surgery was performed. Five patients underwent valve replacement with prosthetic valves, but 1 patient underwent excision of the abscess cavity without valve replacement. There was no operative mortality. All patients continued antibiotic treatment for at least 3 months postoperatively. The median duration of follow-up after surgery was 12 months. During the follow-up period, 1 patient died, while the others remained alive with no recurrences. CONCLUSION: Prosthetic valve replacement is a safe procedure in patients with Brucella endocarditis. Surgical interventions combined with triple antibiotic therapy yield good results with no recurrence in the long-term follow-up.

Plasma homocysteine concentration in patients with poor or good coronary collaterals.

BACKGROUND: Elevated plasma homocysteine (Hcy) concentrations are associated with an increased risk of vascular disease. Hcy is known to inhibit endothelial cell proliferation in vitro. The purpose of the present study was to investigate the role of plasma Hcy concentrations on development of collateral circulation in single-vessel chronic total occlusion. METHODS AND RESULTS: Collateral status was determined by Rentrop's classification. Of 817 patients, 56 cases of pure single-vessel chronic total occlusion were studied. Plasma Hcy concentrations in patients with single-vessel total coronary occlusion were higher compared with controls (17.3 +/-12.6 micromol/L vs 10.9+/-4.9 micromol/L, p=0.015). There was no significant difference in plasma Hcy concentrations of the good and poor collateral groups (17.2+/-13.7 micromol/L vs 15.3+/-9.3 micromol/L, p=0.834). Plasma Hcy concentrations in individual Rentrop subclasses 0, 1, 2 and 3 were as follows: 15.9 +/-9.1, 16.3+/-12.4, 17.1+/-14.1 and 20.1+/-13.5 micromol/L (p=0.893). There was a positive linear correlation between Rentrop subclass and angina pectoris duration (r=0.41, p=0.003). Angina pectoris duration was the only independent variable affecting the development of coronary collaterals in the present study (odds ratio [confidence interval]: 1.85 [1.12-2.91], p=0.014). CONCLUSION: Patients with single-vessel chronic total occlusion had higher plasma Hcy concentrations than controls, but similar Hcy concentrations when compared according to the presence of poor or good coronary collaterals. There is a lack of association between plasma Hcy concentration and coronary collateral status in the current study.

Effect of tirofiban therapy on ST segment resolution and clinical outcomes in patients with ST segment elevated acute myocardial infarction undergoing primary angioplasty.

BACKGROUND: In our study, we assessed the effect of glycoprotein (GP) IIb/IIIa receptor inhibition on microvascular flow after acute coronary occlusion using the early sum of ST segment resolution in electrocardiography. Platelets may play a major role in the dissociation of epicardial artery recanalization and tissue level reperfusion, referred to as the 'no-reflow phenomenon'. Therefore, GP IIb/IIIa receptor inhibition might improve myocardial reperfusion, distinct from its effects on epicardial patency. METHODS AND RESULTS: One hundred and fifteen patients (mean age 57.7 +/- 12.2 years, 96 males, 19 females) with < or = 12-hour acute ST segment elevation myocardial infarction who underwent successful primary percutaneous coronary intervention were retrospectively enrolled into the study. Patients were grouped according to whether they received tirofiban therapy or not. Clinical and electrocardiographic parameters were evaluated. The first sum of ST segment elevation amounts in millimeters was obtained immediately before angioplasty and the second 60 min after restoration of thrombolysis in myocardial infarction III flow. The difference between the two measurements was accepted as resolution of the sum of ST segment elevation and expressed as SigmaSTR. There were no significant differences between the groups regarding age, gender, cardiovascular risk factors, and laboratory parameters, duration from angina onset to the emergency unit, and from door to angioplasty. SigmaSTR was higher in patients who received tirofiban than in those who did not (7.2 +/- 2.8 and 4.2 +/- 2.6 mm, respectively; p < 0.001). There was a significant and positive correlation between GP IIb/IIIa inhibition and SigmaSTR (r = 0.336, p < 0.001), as well as between ejection fraction and SigmaSTR (r = 0.310, p < 0.001). GP IIb/IIIa inhibition was the only independent determinant of SigmaSTR in a multivariate linear regression model which contains 10 variables (p < 0.001). The incidence of in-hospital post-myocardial infarction refractory angina, reinfarction, and heart failure was significantly lower in the tirofiban group (p < 0.05, p < 0.05, and p < 0.05, respectively). Additionally, after 30 days, reinfarction and heart failure were lower in the tirofiban group (p < 0.05 and p < 0.05, respectively). CONCLUSIONS: It is well known that SigmaSTR determines microvascular perfusion. This study shows that GP IIb/IIIa inhibition with tirofiban is of value in preserving microvascular perfusion after restoring coronary thrombolysis in myocardial infarction III flow.