Mortality in acromegaly can be successfully reduced, provided patients are treated using a multimodal approach with careful management of comorbidities.

Factors that can impact medication include patient-related factors, social- and economic-related factors, health system/health care team-related factors, and therapy-related factors. Overall, a multifaceted approach is needed to improve medication adherence. Important components include (1) patient education on hypertension, its treatment modalities and its long-term complications; and (2) patient engagement building on the foundation of education. The various interventions tested have engaged patients through interactive educational sessions, health coaching, motivational interviewing, stage of change behavioral counseling, and pharmacist hypertension management. Strategies utilizing patient education and engagement are needed to improve medication adherence and blood pressure control.

Background: Lambl's excrescences (LEx) are detected by transesophageal echocardiography (TEE) and are characterized as thin, elongated, and hypermobile structures located at the leaflets' coaptation point of the heart valves. The association of LEx with cerebrovascular disease (CVD) is still undefined and yet patients with LEx and suspected CVD receive unproven effective antiplatelet or anticoagulant therapy or even undergo valve surgery. Also, the association of LEx with aging and atherogenic, inflammatory, or thrombogenic parameters has not been reported. Methods: Seventy-seven patients with systemic lupus erythematosus (SLE) (71 women, age 37 ± 12 years) and 26 age- and sex-matched healthy controls (22 women, age 34 ± 11 years) prospectively underwent routine history and physical exam, transcranial Doppler, brain MRI, TEE, carotid duplex, and clinical and laboratory evaluations of atherogenesis, inflammation, platelet activity, coagulation, and fibrinolysis. Subjects without stroke/TIA on enrollment (with and without LEx) had a median follow-up of 57 months. Results: On enrollment, 33 (43%) of 77 patients had CVD manifested as acute stroke/TIA (23 patients), cerebromicroembolism by transcranial Doppler (17 patients), or cerebral infarcts by MRI (14 patients). Mitral or aortic valve LEx were equally frequent in healthy controls (46%) as in patients with and without any CVD (39 and 43%), stroke/TIA (35 and 43%), cerebromicroembolism (41 and 42%), or cerebral infarcts (36 and 43%) (all p ≥ 0.72). Also, other mechanisms for CVD other than LEx such as Libman-Sacks vegetations, patent foramen ovale or interatrial septal aneurysm, aortic or carotid atherosclerosis, or thrombogenesis were found in ≥94% of patients with CVD. In addition, 36 subjects with and 44 without LEx had similar low incidence of stroke/TIA (1 (1.3%) and 2 (2.5%), respectively, p = 1.0) during follow-up. Finally, LEx were not associated with aging, atherogenic risk factors, atherosclerosis, inflammation, or thrombogenesis. Conclusions: In this study, LEx are similarly prevalent in healthy controls and SLE patients, are not associated with CVD, and are not associated with pathogenic risk factors. Therefore, the study findings suggest that LEx may not be cardioembolic substrates, may not represent pathologic valve structures, and may not require therapy.

This article presents the case of a 53-year-old man who presented with acute right superficial femoral and popliteal arterial thrombosis for which he underwent an emergent uncomplicated thrombectomy. He denied preceding cardiovascular or neurologic symptomatology and had no history of coronary or peripheral arterial disease, trauma, hypercoagulability, or malignancy. However, he reported having several days of intense emotional stress prior to presentation. His cardiac exam was normal, his electrocardiogram showed normal sinus rhythm and nonspecific ST-T wave abnormalities, and his troponin levels were normal. Transthoracic echocardiography (TTE) revealed a large (2.4 × 2 cm) apical left ventricle (LV) thrombus, LV apical akinesis, and LV ejection fraction of 40% to 45%. Coronary angiography revealed only luminal irregularities. A repeat TTE performed 3 days after initiating unfractionated heparin revealed complete resolution of the LV thrombus. The patient had an uneventful clinical course and was discharged home in stable condition on oral anticoagulants. The lower incidence of LV thrombus in takotsubo cardiomyopathy (TC) of 1.3% in comparison to 4% to 8% in acute myocardial infarction due to coronary artery disease in the current era of early reperfusion may be explained by the lower extent of ischemic myocardial necrosis associated with TC. This case suggests that the lower extent of myocardial necrosis in TC may also lead to faster resolution of LV thrombus. Therefore, earlier follow-up with TTE (within 2 weeks) and shorter duration of anticoagulation (<3 months) may be considered in patients with TC complicated by LV thrombus formation with or without systemic embolism.

Aortic atherosclerosis (AoA) defined as intima-media thickening or plaques and aortic stiffness (AoS) also considered an atherosclerotic process and defined as decreased vessel distensibility (higher pulse pressure to achieve similar degree of vessel distension) are common in patients with SLE. Immune-mediated inflammation, thrombogenesis, traditional atherogenic factors, and therapy-related metabolic abnormalities are the main pathogenic factors of AoA and AoS. Pathology of AoA and AoS suggests an initial subclinical endothelialitis or vasculitis, which is exacerbated by thrombogenesis and atherogenic factors and ultimately resulting in AoA and AoS. Computed tomography (CT) for detection of arterial wall calcifications and arterial tonometry for detection of increased arterial pulse wave velocity are the most common diagnostic methods for detecting AoA and AoS, respectively. MRI may become a more applicable and accurate technique than CT. Although transesophageal echocardiography accurately detects earlier and advanced stages of AoA and AoS, it is semi-invasive and cannot be used as a screening method. Although imaging techniques demonstrate highly variable prevalence rates, on average about one third of adult SLE patients may have AoA or AoS. Age at SLE diagnosis; SLE duration; activity and damage; corticosteroid therapy; metabolic syndrome; chronic kidney disease; and mitral annular calcification are common independent predictors of AoA and AoS. Also, AoA and AoS are highly associated with carotid and coronary atherosclerosis. Earlier stages of AoA and AoS are usually subclinical. However, earlier stages of disease may be causally related or contribute to peripheral or cerebral embolism, pre-hypertension and hypertension, and increased left ventricular afterload resulting in left ventricular hypertrophy and diastolic dysfunction. Later stages of disease predisposes to visceral ischemia, aortic aneurysms and aortic dissection. Even earlier stages of AoA and AoS have been associated with increased cardiovascular and cerebrovascular morbidity and mortality of SLE patients. Aggressive non-steroidal immunosuppressive therapy and non-pharmacologic and pharmacologic interventions for control of atherogenic risk factors may prevent the development or progression of AoA and AoS and may decrease cardiovascular and cerebrovascular morbidity and mortality in SLE.