To verify the impact of severe obesity (defined as body mass index > 31 kg/m2) on left ventricular (LV) function, 32 asymptomatic obese but otherwise healthy subjects (16 men; age 38 ± 11 years) voluntarily underwent first-pass and equilibrium 99mTc radionuclide angiography at rest and, in 22 of them, during bicycle supine exercise. Data were compared to those obtained from 10 normal volunteers (age 48 ± 13; p < 0.05, vs. obeses). End-diastolic and stroke volumes did not differ between the two groups, whereas end-systolic volume was significantly higher in obese subjects (67 ± 20 vs. 49 ± 20 ml; p < 0.05), and, as a consequence, LV ejection fraction at rest was decreased in obese subjects (59 ± 7%) compared to normals (65 ± 6%; p < 0.05). Due to the higher heart rate in obese subjects (81 ± 13 vs. 69 ± 10 bpm, respectively; p < 0.05) cardiac output was significantly greater compared to normals (7.1 ± 0.8 vs. 6.2 ± 0.2 liters/min, respectively; p < 0.01). During exercise, ejection fraction normally increased in normals (70 ± 7%; p < 0.001, vs. baseline) but not in obese subjects (60 ± 9%; p = nonsignificant vs. baseline). In addition, systolic blood pressure/end-systolic volume ratio was significantly decreased in obese subjects (2.3 ± 1.3) compared to normals (2.8 ± 1.6; p < 0.05). Peak filling rate, normalized to end-diastolic counts per second, was significantly lower in obese subjects (2.2 ± 1.3) compared to normals (2.8 ± 1.6; p < 0.05). This difference was also true when peak filling rate was computed in stroke counts per second (3.8 ± 0.8 in obeses vs. 4.4 ± 0.4 in normals; p < 0.05). Repeat analysis in a subgroup of 10 young obese subjects (age ≤30 years) confirmed decreased ejection fraction at rest (60 ± 4%; p < 0.05) and peak filling rate (2.4 ± 0.4 end-diastolic counts/s; p < 0.05), as well as the lack of ejection fraction increase during exercise (59 ± 9%). Thus, these data indicate a subclinical impairment of LV systolic and diastolic function at rest and during exercise in asymptomatic severely obese but otherwise healthy subjects.
Among acute coronary syndrome (ACS) patients, 15% have concomitant cancer, especially in the first 6 months after their diagnosis, as well as in advanced metastatic stages. Lung, gastric, and pancreatic cancers are the most frequent malignancies associated with ACS. Chemotherapy and radiotherapy exert prothrombotic, vasospastic, and proinflammatory actions. The management of cancer patients with ACS is quite challenging: percutaneous revascularization is often underused, and antiplatelet and anticoagulant pharmacological therapy should be individually tailored to the thrombotic risk and to the bleeding complications. Sometimes oncological patients also show different degrees of thrombocytopenia, which further complicates the pharmacological strategies. The aim of this review is to summarize the current evidence regarding the treatment of ACS in cancer patients and to suggest the optimal management and therapy to reduce the risk of adverse coronary events after ACS in this high-risk population.
summaryBackground: The use of metabolic drugs effective in addition to conventional therapy represents a si&icant challenge in patients with left ventricular dysfunction.
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