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Cardiovascular and cerebrovascular disease are the most common life-threatening disease in the industrialized world. There is high interest in sleep apnea and cardiovascular disease: several studies have demonstrated an association between sleep apnea and cardiovascular and cerebrovascular events. The aim of this review is to critically appraise the possible adverse physiological consequences of sleep apnea on the cardiovascular system and to assess whether such adverse effects constitute a risk for the development of cardiovascular disease.

Background: Several studies showed that there is a state of platelet hyperactivaction in patients with coronary syndrome: the aim of this study is to investigate if the platelet nitric oxide-cyclicGMP (NO-cGMP) pathway, that regulates platelet aggregation is altered in patients with unstable angina (UA) and acute myocardial infarction (AMI)., Methods and Results: Population included 11 patients with UA, 12 patients with AMI and 23 controls. Platelet cGMP was measured by a radioimmunoassay kit, under basal conditions and after stimulation with sodium nitroprusside (SNP), which maximally stimulates soluble guanylate cyclase (sGC), used as an indirect measurement of active sGC. Basal platelet cGMP values were significantly (P<0.001) higher in patients with UA and AMI than in controls (UA, 1089 +/- 412 pmol/10(10) platelets; AMI, 1071 +/- 507 pmol/10(10) platelets; controls, 492 +/- 201 pmol/10(10) platelets). The final cGMP level reached after SNP stimulation was significantly more elevated in UA, compared with both AMI (P<0.05) and controls (P<0.02) (UA, 4428 +/- 2723 pmol/10(10) platelets; AMI, 2728 +/- 655 pmol/10(10) platelets; controls, 2772 +/- 1031 pmol/10(10) platelets); on the contrary no significant difference between AMI and controls was observed., Conclusions: Basal platelet cGMP is significantly higher in both UA and AMI groups. This observation suggests that: (1) platelet-derived NO synthesis may be enhanced inUA and AMI, due to increase of intraplatelet calcium level and of platelet cNOS activation; (2) platelets from UA and AMI patients are continuously stimulated by the high-level NO production due to increased iNOS expression. As far as SNP-dependent cGMP production is concerned, UA and AMI behave as two separate conditions. SNP-stimulated activity in UA is higher than in controls, while a loss of functional sGC is observed in AMI.

We describe the prolonged follow-up of a 64-year-old female patient, with an ectopic intracardiac thyroid gland. The mass was first detected 14 years ago, during a routine echocardiographic examination. The patient suffered from episodes of palpitation and cardiac auscultation revealed a systolic murmur. At cardiac surgery a right ventricular mass penetrating most of the interventricular septum was found. The mass was also prolapsing into the pulmonary infundibulum and could not be removed. On histopathology examination, the presence of a normal tissue was demonstrated. Two main clinical events characterized the prolonged follow-up: the gradual development of a massive tricuspid insufficiency, probably due to the strict anatomic relationship between the septal tricuspid papillary muscle and the mass itself; frequent supraventricular arrhythmias, partially refractory to different pharmacologic regimens, which could be ascribed to the chronic overload of the right atrium. The mass size has been stable over the years, and no thyroid hormone derangement was ever found.

Effectiveness of dual-chamber pacing in patients with dilated cardiomyopathy is still controversial. Our study was performed: to select the most favorable individual atrioventricular (AV) delay; to compare hemodynamic short-term effects in each patient after 2 periods of DDD pacing and sinus rhythm (AV spontaneous); to assess hemodynamic long-term (1 year) effects after DDD pacing at optimum AV delay. In 1996, 9 patients (7 men, 2 women; mean age 69 +/- 5 years) with dilated cardiomyopathy (5 idiopathic, 4 ischemic), NYHA functional class III-IV, ejection fraction < 30%, end-diastolic volume > 60 ml/m2, mitral regurgitation +2/+3, PR interval > or = 200 ms, were enrolled. All patients were implanted with DDD pacemakers and monitored for: ejection fraction and end-diastolic volume (measured by echocardiography and radionuclide angiography); clinical conditions; exercise tolerance and maximum oxygen consumption (by Weber exercise protocol); neurohormonal activity (plasma renin, aldosterone, atrial natriuretic factor). Data were recorded: before DDD implantation; after 2 randomized, single-blind periods of 3 months in VVI mode (at ventricular "sentinel" rate of 50 b/min) and in DDD mode with the optimum AV delay, corresponding for each patient to the minimum end-diastolic volume measured by radionuclide angiography and to the highest cardiac output recorded by echocardiography; after 6 months of DDD pacing with most favorable AV delay. Three more patients died 6 months after (between sixth and twelfth month of follow-up), due to refractory heart failure; 1 patient dropped out because his pacemaker was programmed in VVI mode at low rate, due to intolerance of DDD pacing. Among the other 4 patients no clinical and laboratory parameters were significantly different after 1 year of follow-up. In conclusion, DDD pacing in selected patients with dilated cardiomyopathy showed disappointing results, despite a strict and laboratory monitoring; DDD pacing could be of major benefit in larger populations, according to Doppler mitral flow pattern: those patients with a larger A-wave amplitude could be more sensitive to DDD pacing than those with evidence of poor atrial systole. Moreover, biatral and/or biventricular pacing could also play a significant role.