Early subclinical ventricular dysfunction in patients with insulin resistance.

AIMS: The aim of our study was to evaluate the relationship between insulin resistance and the detection of precocious echocardiographic signs of heart failure in patients with cardiovascular risk factors. METHODS: We enrolled 34 consecutive patients with cardiovascular risk factors. All patients underwent coronary angiography, echocardiography, and laboratory tests. Exclusion criteria were diabetes (fasting glucose greater than 126 mg/dl or treatment with insulin or oral hypoglycemic agents), coronary artery disease, creatinine above 1.5 mg/dl, left-ventricular hypertrophy, valvular heart disease, ejection fraction below 50%, atrial fibrillation, or other severe arrhythmia. The presence of insulin resistance was assessed by using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Ventricular function was investigated by echocardiography. RESULTS: Distinguishing patients with insulin resistance, based on the median value of HOMA-IR (<4.06 and >4.06), we observed that in the group with higher levels of HOMA-IR, there were echocardiographic signs of subclinical ventricular dysfunction statistically more frequent (E/A in group with HOMA <4.06: 1.159 + 0.33 vs. group with HOMA >4.06: 0.87 + 0.29, P = 0.0136; E/E': 6.42 + 4 vs. 15.52 + 3.26, P = 0.001; Tei index: 0.393 + 0.088 vs. 0.489 + 0.079, P = 0.0029; S wave: 0112 + 0.015 vs. 0.114 + 0.027, P = 0.0001; ejection fraction 59.11 + 4.75 vs. 58.88 + 6.81, P = 0.9078). Grade II diastolic dysfunction was observed in 5 patients, grade I in 12 patients, and 17 patients had normal diastolic function. On multivariate analysis, HOMA-IR (P = 0.0092), hypertension (P = 0.0287), waist circumference (P = 0.0009), high-density lipoprotein (P = 0.0004), and fasting blood glucose (P = 0.0003) were variables independently associated with diastolic dysfunction. On analysis of covariance, we found that the variables that influence diastolic dysfunction are HOMA-IR, waist circumference, BMI, and age, and that the only variable that influences Tei index is HOMA-IR. CONCLUSION: Insulin resistance is frequently associated with subclinical left-ventricular dysfunction. Patients with cardiovascular risk factors and increased HOMA-IR levels, although without diabetes mellitus, overt coronary artery disease, or hypertensive cardiomyopathy, may represent a target population for screening programs, recommended changes in lifestyle, and possibly the use of pharmacological interventions to prevent the onset of heart failure.

Preclinical atherosclerosis and metabolic syndrome increase cardio- and cerebrovascular events rate: a 20-year follow up.

BACKGROUND: Intima-media thickness (IMT) is a validated marker of preclinical atherosclerosis and a predictor of cardiovascular events. PATIENTS: We studied a population of 529 asymptomatic patients (age 62 ± 12.8 years), divided into two groups of subjects with and without Metabolic Syndrome (MetS). METHODS: All patients, at baseline, have had a carotid ultrasound evaluation and classified in two subgroups: the first one without atherosclerotic lesions and the second one with preclinical atherosclerosis (increased IMT or asymptomatic carotid plaque). Cardiovascular endpoints were investigated in a 20-years follow-up. RESULTS: There were 242 cardiovascular events: 144 among patients with MetS and 98 among in healthy controls (57.4% vs. 35.2%; P < 0.0001). 63 events occurred in patients with normal carotid arteries, while 179 events occurred in patients with preclinical atherosclerosis (31.8% vs. 54.1%; P < 0.0001). Of the 144 total events occurred in patients with MetS, 36 happened in the subgroup with normal carotid arteries and 108 in the subgroup with preclinical atherosclerosis (45% vs. 63.15%; P = 0.009). 98 events occurred in patients without MetS, of which 27 in the subgroup with normal carotid arteries and 71 in the subgroup with preclinical atherosclerosis (22.88% vs. 44.37%; P = 0.0003). In addition, considering the 63 total events occurred in patients without atherosclerotic lesions, 36 events were recorded in the subgroup with MetS and 27 events in the subgroup without MetS (45% vs. 22.88%; P = 0.0019). Finally, in 179 total events recorded in patients with preclinical carotid atherosclerosis, 108 happened in the subgroup with MetS and 71 happened in the subgroup without MetS (63.15% vs. 44.37%; P = 0.0009). The Kaplan-Meier function showed an improved survival in patients without atherosclerotic lesions compared with patients with carotid ultrasound alterations (P = 0.01, HR: 0.7366, CI: 0.5479 to 0.9904). CONCLUSIONS: Preclinical atherosclerosis leads to an increased risk of cardiovascular events, especially if it is associated with MetS.

Association between asymptomatic carotid atherosclerosis and degenerative aortic stenosis.

OBJECTIVE: Degenerative aortic stenosis shows similarities with atherosclerosis. To confirm the hypothesis that aortic stenosis is an "atherosclerosis-like" disease, we investigated the association between degenerative aortic stenosis and atherosclerosis of carotid arteries. METHODS: We studied 270 consecutive patients, 135 with degenerative aortic stenosis (trans-aortic peak velocity ≥ 2 m/sec) and other 135 subjects without aortic valve disease. All patients underwent echocardiography and ultrasound scan of the supra-aortic trunks to assess the presence of plaque and/or intima-media thickening (IMT). RESULTS: Atherosclerosis of carotid arteries (IMT and plaque) was significantly more frequent in patients with aortic stenosis than in controls (95.5% vs. 66.6%, p < 0.0001). The same result was confirmed as concerns carotid plaques (69.6% vs. 42.2%, p < 0.0001). In addition, there was a significant association between aortic stenosis and degenerative carotid plaque (OR = 3.13; 95% C.I. = 1.90-5.17). Thus the presence of a linear correlation between the trans-aortic peak velocity of the cases and the thickness of the plaques and IMT was evaluated by calculating the coefficient of correlation (R = 0.15 for plaque and R = 0.53 for IMT). CONCLUSIONS: The presence of carotid atherosclerosis is associated with degenerative aortic stenosis and the severity of aortic stenosis corresponds to an increase of the thickness of plaque and IMT. This relationship is quite new. Our result strengthens the pathogenetic hypothesis "atherosclerosis-like" of degenerative aortic stenosis and suggest the ultrasound scan as a non invasive method for risk stratification in patient with aortic stenosis, with therapeutic implications especially for higher risk subgroups.

Residual vein thrombosis for assessing duration of anticoagulation after unprovoked deep vein thrombosis of the lower limbs: the extended DACUS study.

The safest duration of anticoagulation after idiopathic deep vein thrombosis (DVT) is unknown. We conducted a prospective study to assess the optimal duration of vitamin K antagonist (VKA) therapy considering the risk of recurrence of thrombosis according to residual vein thrombosis (RVT). Patients with a first unprovoked DVT were evaluated for the presence of RVT after 3 months of VKA administration; those without RVT suspended VKA, while those with RVT continued oral anticoagulation for up to 2 years. Recurrent thrombosis and/or bleeding events were recorded during treatment (RVT group) and 1 year after VKA withdrawal (both groups). Among 409 patients evaluated for unprovoked DVT, 33.2% (136 of 409 patients) did not have RVT and VKA was stopped. The remaining 273 (66.8%) patients with RVT received anticoagulants for an additional 21 months; during this period of treatment, recurrent venous thromboembolism and major bleeding occurred in 4.7% and 1.1% of patients, respectively. After VKA suspension, the rates of recurrent thrombotic events were 1.4% and 10.4% in the no-RVT and RVT groups, respectively (relative risk = 7.4; 95% confidence interval = 4.9-9.9). These results indicate that in patients without RVT, a short period of treatment with a VKA is sufficient; in those with persistent RVT, treatment extended to 2 years substantially reduces, but does not eliminate, the risk of recurrent thrombosis.