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Background: The presence of extracranial artery disease has been used as a predictor of coronary artery disease (CAD). The present study was conducted to test the prevalence of extracranial artery disease among patients with suspected CAD., Methods: Among candidates for coronary arteriography, 400 consecutive patients (mean age 63 +/- 11 years, 78% males, 22% females) underwent color duplex ultrasound of carotid arteries., Results: Extracranial artery disease was documented in 60 patients (15%), CAD in 309 patients (77%). Patients with extracranial artery disease were significantly older (p < 0.001), smoked a higher amount of pack-years (p < 0.001), showed a higher incidence of diabetes (p < 0.01), hypertension (p < 0.05) and CAD (p < 0.05) when compared to extracranial artery disease-free subjects. Plotting age against extracranial artery disease and CAD distribution, extracranial artery disease occurred later in life than CAD (p < 0.001). The best cut-off point of age for predicting extracranial artery disease was 68 years. Carotid angiography was performed in 114 patients after cardiac catheterization (k = 0.8044 with color duplex scanning)., Conclusions: Extracranial artery disease is frequent among patients undergoing coronary arteriography. Carotid ultrasound screening is useful in older patients.

Left ventricular remodeling, through long-term left ventricular chamber dilation and increased wall stress can result in alteration of ventricular architecture and impairment of systolic and diastolic performance. Most of the studies regard post acute myocardial infarction remodeling, knowledge is still lacking about preoperative and postoperative factors which predict the long-term prognosis of patients who underwent venous coronary artery bypass graft surgery. We evaluated 243 patients (225 males, 18 females, mean age 65 +/- 7.3 years) submitted to venous coronary artery bypass graft surgery and 10-year follow-up (123 +/- 20 months). Global mortality was 17.6% (n = 43), significantly higher in patients with ejection fraction (EF) < 50% (log-rank test p < 0.001). The survivors (n = 200) were subdivided into two groups according to postoperative EF: patients with EF > or = 50% (n = 160) and patients with EF < 50% (n = 40). Multivariate analysis revealed that cardiovascular risk factors (hypertension, diabetes, hypercholesterolemia, smoking), number of grafts and infarct location were not associated with EF reduction. Only multivessel disease was significantly associated with EF reduction (p = 0.008). Preoperative echocardiographic parameter analysis evidenced that regional ventricular wall motion score was significantly higher in patients with reduced EF (EF < 50% 11 +/- 7.5; EF > or = 50% 6 +/- 4.1, p < 0.001) and left ventricular dilation (p < 0.001). Multivariate analysis revealed that the strongest correlates of EF < 50% were left ventricular wall motion score index > 10 (odds ratio 5.8, 95% confidence interval 2.8-11.7) and multivessel disease (odds ratio 9.0, 95% confidence interval 2.6-31.08). This study revealed that echocardiographic detection of preoperative ventricular wall motion score may be useful to assess patients at high risk of ventricular remodeling after venous coronary artery bypass graft surgery.

Degenerative aortic stenosis represents the most common form of aortic stenosis. The aim of this study was to evaluate the relationship between symptoms, valvular disease severity and prognosis. We studied the evolution of valvular aortic stenosis in 65 patients (39 males and 26 females, mean age 77.78 +/- 6.2 years) for a period of 7 years. All patients were submitted to accurate anamnestic examination, ECG, color Doppler echocardiography. Sixteen patients (26%) underwent cardiac catheterization. Associated diseases were: hypertension (45%), diabetes (40%), dyslipidemia (29%), chronic obstructive lung disease (6%). In 64% patients, the diagnosis of aortic stenosis was made after symptoms onset, and in 36% was occasional. Mean age at symptoms onset was 70 +/- 17 years: dispnoea was present in 81%, chest pain in 32%, and syncope in 8%. At the beginning of the follow-up, echocardiography showed, aortic stenosis to be mild in 21.73%, moderate in 60.8% and severe in 17.4%. At the end of the follow-up, mild stenosis was present in 9.5%, moderate in 38.7%, and severe in 51.8%. At entry, 56.6% had pure aortic stenosis, 34.78% had steno-insufficiency and 8.7 had an associated mitral valve insufficiency. At the end of the follow-up pure aortic stenosis was present in 17%, steno-insufficiency in 40%, and associated mitral valve insufficiency in 4.3%. Surgery was performed in 21% of the patients (77% valve replacement and 23% valve replacement and aortocoronary bypass). The mortality, at the end of the follow-up, was 31%. Causes of death were: heart failure (61%), arrhythmias (23%), and surgical complications (16%).(ABSTRACT TRUNCATED AT 250 WORDS)

In the progression from myocardial hypertrophy to heart failure, abnormalities in the interstitial space of the heart seem to play a critical role. The formation of an extracellular oedema and the alterations in coronary subendocardial perfusion are associated with the development of interstitial fibrosis. Cardiac experimental studies documented the presence of augmented interstitial fluid volume and pressure and a subsequent remodelling of the fibrillar network of the extracellular space of the myocardium during the phases of the cardiovascular response to a sudden overload. Variations of the Starling's forces balance caused by enhanced endothelial permeability or due to an impairment of cardiac lymphatic drainage may contribute to the development of an acute heart failure. During stable hyperfunction, the organization of a chronic oedema should account for interstitial changes in the hypertrophic myocardium. Reactive fibrosis seems to be under hormonal control. The activation of the renin-angiotensin-aldosterone system is responsible for interfascicular and intercellular accumulation of fibrillar collagen within the cardiac interstitium. Perivascular fibrosis in the subendocardium may impair intramyocardial distribution of coronary flow. When an inadequate hypertrophy occurs, because of an elevation in ventricular wall stress, myocardial oxygen consumption rises and this may lead to the exhaustion of coronary blood flow reserve in the subendocardial layers. This underperfusion may be responsible for the development of myocardial ischemia. Coronary hemodynamic changes in the microcirculation as those prompted by interstitial alterations may contribute to the onset of myocyte necrosis and to the formation of restorative fibrosis. The progressive mechanical overload of the spared hypertrophied myocytes could explain the initiation of a positive feedback mechanism which perpetuates endomyocardial perfusion impairment, interstitial oedema and remodelling, finally, causing myocyte deaths and fibrous tissue proliferation. These structural alterations and their pathophysiological counterparts appear to be closely related to the evolution from compensatory hypertrophy to chronic myocardial failure in hypertrophic heart disease.