No abstract

No abstract

A 52-year-old man was referred to our intensive care unit by the emergency department for chest pain and severe recent-onset dyspnea. The patient had no particular medical history and no cardiovascular risk factors. His complaints started 3 weeks previously after what he described as a severe flu with cough and fever.At clinical examination, the patient was breathless with a respiratory rate of 28 cycles per minute and a fever of 38.3°C. His heart rate was 88 bpm and blood pressure was 112/ 68 mm Hg. Pulmonary auscultation revealed bilateral wet rales in the lower lung fields. An ECG showed no particularities. Biology found a frank inflammatory syndrome with an erythrocyte sedimentation rate of 90, a C-reactive protein of 180 mg/L, and a white blood cell count of 14 500. His troponin I level was 6.4 mg/L and BNP level was 6788 pg/mL.Transthoracic echocardiography performed at admission (Figure 1 and Movie I of the online-only Data Supplement) showed a severely depressed left ventricular function with an ejection fraction of Ϸ30%, along with a massive apical adherent thrombus. Another spherical, highly mobile, pedunculated thrombus was observed, as well as a circumferential pericardial effusion and an important pleural effusion.Given the potentially high risk of distal embolization, an urgent surgery was discussed; meanwhile, the patient was treated with unfractionated heparin. A second echocardiographic control was performed just 1 hour later, which showed an impressive live preprocedural migration of the mobile thrombus from the left ventricular apex toward the outlet chamber and through the aortic orifice to the systemic circulation (Figure 2 and Movie II of the online-only Data Supplement). Extraordinarily and fortunately, no symptomatic embolic event was noted. A whole-body computed tomography scan showed no signs of infarction or embolization; Doppler echocardiography of the lower limbs and renal arteries also proved normal, as did the coronary angiogram. The final presumptive diagnosis of acute myocarditis complicated by an asymptomatic embolization was made. Anticoagulation with unfractionated heparin was continued, but surgery was canceled. The evolution was favorable, with rapid clinical improvement and partial recovery of ventricular function with a notable reduction in thrombus size. U.S. was discharged home on day 10 with angiotensin-converting enzyme inhibitors, ␤-blockers, diuretics, and Coumadin. On the control performed 1 month later, he was completely symptom free, and echocardiography revealed no abnormalities (Figure 3 and Movie III of the online-only Data Supplement).

Coronary artery spasm can be induced at DSE, but is a rare finding; it could, though, be clinically relevant as it may partly explain some erroneously labelled 'false-positive' examinations. Methylergometrine provocation test is a safe and advisable approach in such situations.

No abstract

Diabetes mellitus has been associated with changes in the structure and function of the myocardium manifesting in the early stages of the disease as subtle systolic and diastolic dysfunction; the role of dobutamine stress echocardiography (DSE) in this setting remains unclear. We sought to evaluate the prevalence of dobutamine-induced systolic dysfunction amongst diabetic patients with normal at rest left ventricular ejection fraction and no coronary artery disease and to investigate whether an optimized therapeutic approach can reverse these abnormalities. 1,363 patients with DM referred to our echocardiography laboratory for DSE between January 2008 and June 2010 were prospectively investigated. Patients with normal left ventricular ejection fraction (LVEF) at rest and significant deterioration during peak dobutamine infusion (defined as a ≥10% decrease) in the absence of coronary artery disease or vasospasm were enrolled. They received on top of their usual treatment 5 mg perindopril and had their glycemic control intensified. At 60 days, all of them were controlled for clinical status and underwent a control DSE. 18 patients were included, there were 9 males and 9 females, mean age was 66.1 ± 10.2 years. All the patients had type II DM with a mean duration of 12.7 ± 6.6 years. They all had normal at rest echocardiographic findings with no wall motion abnormalities; mean LVEF was 62 ± 6%. At peak dobutamine, LVEF significantly deteriorated in all the patients with a mean 15 ± 5% decrease compared to baseline. After therapeutic optimization, Glycated haemoglobin improved from 8.53 ± 2.05% to 6.8 ± 0.6% (δ HbA1C = 1.73%, P = 0.001), mean LVEF at peak dobutamine infusion evolved from 47.17 ± 4.2% pre-optimization to 58 ± 4.8% at control (10.83% improvement; P < 0.001). In patients with DM and normal at rest LVEF, Dobutamine infusion during DSE can induce a significant deterioration in LVEF in the absence of coronary artery disease or vasospasm. This specific condition could be largely reversed through an optimized therapy based on a tighter metabolic control and a more stringent renin-angiotensin-aldosterone system inhibition.

No abstract

No abstract