Prothrombotic profile in patients with vasospastic or non vasospastic angina and non significant coronary stenosis.

BACKGROUND: Patients with vasospastic (VA) or non vasospastic angina (NVA) without significant coronary stenosis have a reduced risk of infarction but is unclear whether or not this may be attributable to a lack of prothrombotic profile - similar to that present in patients with stable coronary artery disease (CAD). METHODS: Plasma levels of von Willebrand factor, total and free tissue factor pathway inhibitor, plasminogen activator inhibitor-1, and fibrinogen were analyzed in 15 patients with stable VA and 23 with NVA, all with vasoconstrictive response to acetylcholine although with different severity. Results were compared with those of 20 age-matched controls and 10 patients with CAD. RESULTS: Plasma levels of von Willebrand factor in patients with VA or NVA were higher than in controls (207 ± 62 and 203 ± 69% vs 121 ± 38%, p < 0.001) and tended to be lower than in CAD patients (264 ± 65, p = 0.145). They also presented higher total tissue factor pathway inhibitor (123 ± 18 and 111 ± 25 vs 88 ± 14, ng/ml p < 0.001) and plasminogen activator inhibitor-1 levels than controls (51 ± 30 and 52 ± 31% vs 19 ± 9 ng/ml, p < 0.001) and similar to CAD patients (134 ± 23 and 62 ± 31, respectively, ns). Moreover, free tissue factor pathway inhibitor plasma levels were lower than controls (18 ± 5 and 17 ± 5 vs 23 ± 8 ng/ml, p = 0.002) and similar to CAD patients (14 ± 5, ns). Despite this prothrombotic condition none of VA or NVA patients presented a myocardial infarction during a 9 year follow-up, an observation also reported in larger series. CONCLUSIONS: During a stable phase of their disease, patients with VA or NVA present a prothrombotic profile that might eventually contribute to occurrence of myocardial infarction. The rarity of these events, however, may suggests that ill defined factors would protect these patients from coronary plaque rupture/fissure.

Late benefits of dual-chamber pacing in obstructive hypertrophic cardiomyopathy: a 10-year follow-up study.

OBJECTIVE: To examine the mid-term and long-term outcomes in patients with obstructive hypertrophic cardiomyopathy (HCM) submitted to pacing. DESIGN: Prospective, observational study. SETTING: Single, non-referral centre. PATIENTS AND INTERVENTION: Fifty patients (62 + or - 11 years) with HCM refractory to medical treatment, all in New York Heart Association (NYHA) class III or IV, and with a rest gradient >50 mm Hg underwent a dual-chamber pacemaker implantation. Patients were followed-up for up to 10 years (mean 5.0 + or - 2.9, range 0.6-10.1). RESULTS: During the first year of follow-up, rest gradients decreased (baseline 86 + or - 29 mm Hg; 3 months 55 + or - 37; l year 41 + or - 26; p=0.0001). NYHA class improved, as well as exercise tolerance (baseline 281 + or - 112 m; 3 months 334 + or - 106 m; 1 year 348 + or - 78 m; p<0.0001). The physical and mental components of the quality of life instrument SF-36 also improved. Left ventricular wall thickness remained unchanged, while ejection fraction decreased (baseline 76 + or - 10%; 3 months 74 + or - 8%; 1 year 66 + or - 13%; p=0.002). During the long-term follow-up, an additional reduction in obstruction was found (final rest gradient 28 + or - 24 mm Hg, p<0.02). Those patients who did not improve to NYHA class I or II and continued to have obstruction were given other treatments (six, alcohol ablation; three, surgical myectomy). CONCLUSIONS: Pacing in HCM results in a significant reduction in obstruction, improvement of symptoms and exercise capacity that is progressive and may be achieved after a long period of time. In this series, only 18% of cases needed a more aggressive treatment to relieve residual obstruction and obtain a satisfactory symptomatic status. In conclusion, these results emphasise the need for new controlled studies of pacing with a longer follow-up.

Clinical and neurohumoral consequences of diuretic withdrawal in patients with chronic, stabilized heart failure and systolic dysfunction.

BACKGROUND: Loop diuretics are beneficial in heart failure in the short term because they eliminate fluid retention, but in the long-term, they could adversely influence prognosis due to activation of neurohumoral mechanisms. AIMS: To explore the changes induced by diuretic withdrawal in chronic nonadvanced heart failure. METHODS: Diuretics were withdrawn in 26 stabilized heart failure patients with systolic dysfunction (ejection fraction [EF]<45%). Clinical status was evaluated by physical exam, exercise capacity (corridor test) and New York Heart Association (NYHA) class. Biochemical and neurohumoral determinations were performed at baseline and at 3 months. RESULTS: At 3 months, 17 out of 26 patients (65%) were able to tolerate diuretic interruption without a deterioration in exercise capacity or New York Heart Association functional class. Renal function parameters improved (baseline urea 46.2+/-10.8 to 39.2+/-10.1 mg/dl at 3 months, p=0.014; creatinine 1.1+/-0.23 to 0.98+/-0.2 mg/dl, p=0.013). Glucose metabolism also improved (fasting glucose 151+/-91 to 122+/-14 mg/dl, p=0.035). Heart rate and systolic blood pressure did not significantly change, while diastolic blood pressure increased (from 80+/-10 to 87+/-13 mm Hg, p=0.006). Neurohumoral determinations showed a decrease in plasma renin activity (4.19+/-5.96 to 2.88+/-4.98 ng/ml, p=0.026), with no changes in aldosterone, arginine-vasopressin, endothelin-1 and norepinephrine. In contrast, atrial natriuretic peptide significantly increased (115+/-87 to 168+/-155 pg/ml, p=0.004). CONCLUSION: Diuretic withdrawal in stabilized heart failure with systolic dysfunction is associated with an improvement in renal function parameters, glucose metabolism and some neurohumoral parameters, such as plasma renin activity; however, atrial natriuretic peptide levels increased.