Tako-tsubo cardiomyopathy observed in a patient with sepsis and transient hyperthyroidism.

A 55-years-old woman, with a history of hypertension and ischemic stroke with residual left hemiparesis, was admitted to our hospital because of dyspnoea with clinical evidence of acute pulmonary edema. She was found to have a sinus tachycardia with ST-elevation in leads D1, aVL and V1-V4 in the electrocardiogram, and akinesis of the left ventricular apex with overall left ventricular systolic function being severely impaired and an ejection fraction of 28% on echocardiography. Orotracheal intubation was performed and mechanical ventilation was immediately started. Emergency cardiac catheterization was performed 2 h after the symptom onset. Coronary angiography showed no significant coronary artery disease. Blood analysis revealed an increase in the creatine kinase MB fraction, a significant positive detection in troponin T, a white blood cell count of 35000 per microliter, C-reactive protein of 59,9 mg/dl, and transient elevation in the concentration of free triiodothyronine, free thyroxine, thyroid globulin antibody, and thyroid peroxidase antibody. The symptoms improved during the next days, and follow-up echocardiography 18 days later showed complete resolution of the left ventricular dysfunction. These data suggest that tako-tsubo cardiomyopathy may be induced in patients with sepsis and transient hyperthyroidism.

Exercise induced atrio-ventricular (AV) block during nuclear perfusion stress testing: a case report.

BACKGROUND: Exercise causes enhanced sympathetic discharge and results in physiologic tachycardia. However, in some patients with a diseased conduction system resulting from acute ischemia, exercise can precipitate heart block. METHODS AND RESULTS: In this report we describe a 51 years old male patient with transient advanced degree atrioventricular (AV) block developed during recovery from exercise stress testing, resolved after the administration of atropine. Nuclear perfusion imaging demostrated stress-induced ischemia of the inferior-apical segments, and recovery of perfusion in the images obtained at rest. Coronarography showed critical stenosis of the right coronary artery, which was treated by percutaneous coronary intervention (PCI) and drug eluting stent (DES) deployment. CONCLUSION: Nuclear myocardial perfusion imaging provides noninvasive evidence that transient ischemia of the infero-apical segment can result in advanced degree AV block in patient with critical severe right coronary disease.

Effect of physical training on exercise capacity, gas exchange and N-terminal pro-brain natriuretic peptide levels in patients with chronic heart failure.

BACKGROUND: Decreased exercise capacity is the main factor restricting the daily life of patients with chronic heart failure. N-terminal pro-brain natriuretic peptide (NT pro-BNP) is strongly related to the severity of and is an independent predictor of outcome in chronic heart failure. DESIGN: The study aimed to evaluate the effect of exercise training on functional capacity and on changes in NT pro-BNP levels and to assess the effect of exercise training on quality of life. MATERIALS AND METHODS: Sixty patients (45 men/15 women, mean age 52.7 years; +/-5.3 SD), with stable heart failure (45 ischaemic/hypertensive and 15 idiopathic patients), in New York Heart Association (NYHA) functional class II (n=35) to III (n=25), with an ejection fraction less than 40%, were randomly assigned to a training (n=30) and a control group (n=30). The training group (30 patients) performed 3 months of supervised physical training programme using a bicycle ergometer for 30 min three times a week at a load corresponding to 60-70% of their oxygen consumption (VO2) peak. The control group did not change their previous physical activity. A graded maximal exercise test with respiratory gas analysis and an endurance test with constant workload corresponding to 85% of the peak oxygen load at the baseline and after 3 months were performed, and at the same times NT pro-BNP levels were measured. RESULTS: The exercise capacity increased from 15.8 (+/-2.3 SD) to 29.9 (+/-2.1 SD) min (P<0.0001) and the peak VO2 tended to improve from 14.5 (+/-1.4 SD) to 17.7 (+/-2.6 SD) ml/kg per min (P<0.0001) during the supervised training period. VO2 at the anaerobic threshold increased from 12.9 (+/-1.0 SD) to 15.5 (+/-1.7 SD) ml/kg per min (P<0.0001). NT pro-BNP levels decreased from 3376 (+/-3133 SD) to 1434 (+/-1673 SD) pg/ml (P=0.043). The positive training effects were associated with an improvement in the NYHA functional class. CONCLUSION: Physical training of moderate intensity significantly improves the exercise capacity and neurohormonal modulation in patients with chronic heart failure. This is associated with an alleviation of symptoms and improvement in quality of life.

Cystatin C levels are decreased in acute myocardial infarction: effect of cystatin C G73A gene polymorphism on plasma levels.

BACKGROUND: Cystatin C is the most abundant protease inhibitor in the plasma. Low plasma levels have been found in patients with aortic aneurysms and they seem correlated with the extension of the aortic lesions in early aneurysms detected by ultrasonography. METHODS: In this study, plasma levels of cystatin C have been investigated in patients with acute myocardial infarction (AMI), unstable angina and controls. The effect on plasma levels of the G73A polymorphism of the CST3 gene has been also evaluated. RESULTS: Patients with acute myocardial infarction showed significantly lower levels of cystatin C compared to unstable angina and controls, but levels were nearly normal in a week after the acute event. The genotype distribution of the G73A polymorphism was not different among the groups. Nevertheless, cystatin C levels decreased proportionally with the number of A alleles. Cystatin C levels were positively correlated with age, triglyceride/HDL cholesterol ratio and creatinine, and negatively with HDL cholesterol and the number of A alleles. All variables, but not HDL cholesterol, were independently correlated in a multivariate analysis. CONCLUSIONS: Cystatin C is decreased in acute myocardial infarction. It is still not clear whether lower cystatin C levels are causally linked to the acute event or just represent a negative acute phase response. The CST3 gene G73A polymorphism functionally affects cystatin C plasma levels.

[Efficacy and safety of non-invasive positive pressure ventilation therapy in acute pulmonary edema]. / Efficacia e sicurezza della terapia con ventilazione a pressione positiva non invasiva nell'edema polmonare acuto.

BACKGROUND: Non-invasive positive pressure ventilation (NIPPV) is an effective treatment for acute respiratory failure in patients with chronic obstructive pulmonary disease. We assessed the efficacy and safety of this therapy in acute cardiogenic pulmonary edema (ACPE). METHODS: In addition to routine therapy consisting of oxygen, nitrates and diuretics, 60 patients (39 male, 21 female, mean age 72.5 +/- 15.8 years) were started on full mask NIPPV using a Sullivan VPAP II ventilator delivering pressure support 15 cm H2O, PEEP 5 cm H2O, FiO2 100%. Pressure support were titrated to achieve oxygen saturation (SaO2) > 95%. Physiological measurements were obtained in the first 2 h and at 3 h, 4 h, and 10 h. Outcome measures included arterial blood gas (ABG), Borg dyspnea score, vital signs, and need for endotracheal intubation (ETI). RESULTS: Initial mean values on FiO2 100% by non nonrebreather mask: pH 7.11 +/- 0.25, paCO2 67.7 +/- 17.5 mmHg, paO2 71.5 +/- 29.7 mmHg, SaO2 83 +/- 12%, lactate concentrations 4.7 +/- 2.3 mmol/L, Borg score 8.6 +/- 1.3, respiratory rate (RR) 41 +/- 7. At 60 minutes of NIPPV, improvement was statistically significant: pH 7.35 +/- 0.18 (difference 0.24; p < 0.0001), paCO2 43 +/- 13 mmHg (difference 24.7; p < 0.0001), paO2 102 +/- 10 mmHg (difference 30.5; p < 0.0001), SaO2 99 +/- 5% (difference 16; p < 0.0001), lactate concentrations 1.2 +/- 0.8 (difference 3.5; p < 0.0001) Borg score 3.6 +/- 0.9 (difference 5; p < 0.0001), RR 24.6 +/- 5 (difference 17.1; p < 0.0001). NIPPV duration ranged from 40 minutes to 24 hours (median 3 hours, 30 minutes). Fifty-six patients (93.4%) improved allowing cessation of NIPPV. ETI was required in four (6.6%) of 60 patients. There were non complications of NIPPV. CONCLUSION: In this study of acute cardiogenic pulmonary edema, NIPPV is an effective treatment and may help prevent ETI.