Mauro Cardillo

Troponin I release after intravenous treatment with high furosemide doses plus hypertonic saline solution in decompensated heart failure trial (Tra-HSS-Fur)

BACKGROUND High values of cardiac troponin in acute decompensated congestive heart failure (ADHF) identify patients at higher risk and worsened prognosis. A cardiac troponin increase during therapy indicates the need for more appropriate intervention, aimed at compensating cardiac disease and effectively minimizing myocardial wall stress and subsequent cytolysis. This study evaluated the effects of an intravenous high dose of furosemide with (group A) or without small volume hypertonic saline solution (HSS) (group B) on myocardial cytolysis in patients with ADHF. METHODS A total of 248 consecutive patients with ADHF (148 men, mean age 74.9 ± 10.9 years) were randomly assigned to group A or B. Plasma levels of cardiac troponin-I, brain natriuretic peptide, glomerular filtration rate by Modification of Diet in Renal Disease formula, bioelectrical impedance analysis measurements, and delta pressure/delta time (dP/dt) rate were observed on admission and discharge for all patients. RESULTS We observed a significant reduction of cardiac troponin in both groups and a significant improvement in renal function, hydration state, pulmonary capillary wedge pressure (P < .0001), end diastolic volume (P < .01), ejection fraction (P < .01), and dP/dt (P < .004) in group A. We also observed a significant reduction in body weight (64.4 vs 75.8 kg) (P < .001), cardiac troponin I (0.02 vs 0.31 ng/mL) (P < .0001) and brain natriuretic peptide (542 vs 1,284 pg/mL) (P < .0001), and hospitalization time (6.25 vs 10.2 days) (P < .0001) in the HSS group. CONCLUSIONS These data demonstrate that intravenous high doses of furosemide do not increase myocardial injury and, in addition, when associated to HSS, significantly reduce cardiac troponin I release. This behavior is mirrored by the achievement of improved hemodynamic compensation at echocardiography and body hydration normalization.

One-year renal and cardiac effects of bisoprolol versus losartan in recently diagnosed hypertensive patients: a randomized, double-blind study.

AbstractBackground and objectives: Hypertension is a significant cause of chronic renal injury and its effective treatment is capable of reducing the rate of renal failure. β-Adrenoceptor antagonists (β-blockers) have been reported to induce a deterioration in renal function, while several data have indicated a renoprotective effect of treatment with the angiotensin II type 1 receptor antagonist losartan. Previous studies of the interaction between the selective β1-blocker bisoprolol and kidney function were performed only for short-and medium-term periods. The aim of this study was to compare the antihypertensive efficacy and renal and cardiac haemodynamic effects of bisoprolol with those of losartan over a 1-year time period in patients with essential hypertension. Methods: Seventy-two patients (40 males) with recently diagnosed uncomplicated (European Society of Hypertension [ESH] criteria stage 1–2) hypertension (mean ± SD age 52 ± 12 years) were enrolled in the study. After a run-in period of 14 days on placebo, the patients were randomized in a double-blind, prospective study to receive either bisoprolol 5 mg or losartan 50 mg, administered once daily for 1 year. At recruitment and 12 months after treatment, cardiac output and renal haemodynamics and function were evaluated by echocardiography and radionuclide studies, respectively. Results: There were no significant differences in baseline clinical data, including glomerular filtration rate and blood pressure, between the two treatment groups. At 1 year, blood pressure had decreased significantly (p < 0.001) with both treatments, and heart rate was reduced only in the group taking bisoprolol. The long-term effects on renal haemodynamics and cardiac function were similar with both drugs, the only change being a significant reduction in the filtration fraction for each group. Conclusions: These data suggest that both bisoprolol and losartan are effective agents for the treatment of patients with recently diagnosed ESH stage 1–2 hypertension. Over a 1-year period, both agents maintained good renal and cardiac performance and haemodynamics.

A hidden echocardiographic pitfall: the Gerbode defect

SIMI 2013 The Gerbode defect is characterized by a perimembranous ventricular septal defect (VSD) between the left ventricle and the right atrium. It is a rare defect representing less than 1 % of congenital cardiac defects [1]. Acquired cases have been described, most often due to endocarditis, but also secondary to valvular surgery, thoracic trauma and ischemic heart disease. Frank Gerbode was the first surgeon to report a successful series of patients who underwent surgery for left ventricular to right atrium shunt in 1958 [2]. Gerbode has described two types of defect: ‐ Type A: In this form, the concurrent presence of a perimembranous VSD plus the tricuspid valve defect are visible. The shunt starts from the left ventricle to the right ventricle and through the tricuspid valve into the right atrium. This is referred to as an indirect left ventricle‐right atrium shunt. ‐ Type B: This form is characterized by a left ventricle to the right atrium shunt. This rare form of interventricular septal defect should be suspected during the performance of an echocardiogram, when there is an unusually dilatated right atrium, and when, in the presence of an interventricular septal defect, high velocity flows or aliasing are absent in the right ventricle (mainly in inflow tract) [3]. A particular feature of the Gerbode defect is the high Doppler gradient of the shunt, due to the higher pressure gap between the left ventricle and the right atrium rather than left ventricle‐ right ventricle (especially in the presence of pulmonary hypertension).

Large hiatal hernia at chest radiography in a woman with cardiorespiratory symptoms

Hiatal hernia (HH) is a frequent entity. Rarely, it may exert a wide spectrum of clinical presentations mimicking acute cardiovascular events such as angina-like chest pain until manifestations of cardiac compression that can include postprandial syncope, exercise intolerance, respiratory function, recurrent acute heart failure, and hemodynamic collapse. A 69-year-old woman presented to the emergency department complaining of fatigue on exertion, cough, and episodes of restrosternal pain with less than 1 hour of duration. Her medical history only included some episodes of bronchitis and no history of hypertension. The 12-lead electrocardiogram demonstrated sinus rhythm with right bundle-branch block. Laboratory tests, including cardiac troponin I, were within normal reference values. Chest radiography showed no significant pulmonary alterations and revealed in mediastinum a huge abnormal shadow overlapping the right heart compatible with a gastric bubble.The gastroscopy confirmed a large HH. A 2-dimensional transthoracic echocardiogram, using all standard and modified apical and parasternal views, revealed an echolucent mass, compatible with HH, compressing the right atrium. Also, it showed an altered left ventricular relaxation and a mild increase of pulmonary artery pressure (35 mm Hg). Spirometry showed a mild obstruction of the small airways, whereas coronary angiography showed normal coronary arteries. We concluded that the patients symptomatology was related to the compressive effects of the large hiatal ernia, a neglected cause of cardiorespiratory symptoms. The surgical repair of HH was indicated.

Hiatal herniation of the stomach and pancreas in a patient with oxygen desaturations

Hiatal hernia (HH), a neglected cause of cardiorespiratory symptoms, is a frequent entity characterized by the displacement of the gastro- esophageal junction and part of the stomach into the mediastinum. Although often asymptomatic, HH may also exert a wide spectrum of clinical presentations due to cardio-pulmonary compression, including acute cardiovascular events such as arrhythmias, post-prandial syncope, angina-like chest pain, recurrent acute heart failure, hemodynamic collapse, electrocardiographic changes (T-wave inversion, ST elevation) simulating myocardial ischemia or pericarditis, and respiratory manifestations that can range from exercise intolerance and dyspnea on exertion to alteration of pulmonary function tests. (Published. 4 December 2013) Citation: Libyan J Med 2013, 8 : 23288 - http://dx.doi.org/10.3402/ljm.v8i0.23288

Porcelin and duplicated gallbladder associated with pancreatic cancer

Duplication of the gallbladder is a very rare clinical entity that is due to a congenital anomaly of the hepatobiliary system with a reported incidence of one per 4,000–5,000 persons, first described in a killed victim of the Emperor Augustus in 31 BC. It results from abnormalities in embryogenesis during the fifth and sixth weeks of gestation, and may be associated with some medical or surgical problems related to gallstones and cholecystitis [1] but, only rarely to gallbladder cancer [2]. Accurate pre-operative diagnosis of a double gallbladder is important to prevent possible surgical complications and repeated surgery when cholecystectomy is performed. Additionally, a porcelain gallbladder is another rare biliary condition characterized by the extensive calcification of the wall, sometimes associated with an obstructing cystic duct carcinoma, and is considered as a factor that may predispose to gallbladder cancer, but at a much lower rate than previously estimated [3]. In this brief report, we show a very unusual combination of double biliary anomalies consisting of a duplicated and a porcelain gallbladder. The patient was a 75-year old woman admitted for 3 months history of asthenia, dyspepsia, anorexia, and weight loss (3 kg). Physical examination revealed a hard palpable mass in the right upper quadrant, and laboratory data demonstrated severe anemia (Hb 6.5 mg/dl). Enhanced computed tomography (Fig. 1) to search for malignances, showed a double porcelain gallbladder separated by a shared medial wall, and united in the distal portion of the neck and infundibulum, with a unique main biliary duct. Also pres

Giant left atrium in a woman with mitral prosthetic valve malfunction and history of rheumatic heart disease

A 65-year-old woman with a past medical history of rheumatic heart disease, hypertension, chronic atrial fibrillation and chronic obstructive pulmonary disease was admitted to our department with a chief complaint of cough and shortness of breath worsened in the last month. She had undergone mechanical mitral valve prosthesis replacement for severe mitral regurgitation when she was 42 years old, in 1982. In the emergency department (ED), a chest X-ray study showed a marked prominence of the right cardiac border, nearly complete opacification of the lower lung fields and splaying of the carina (Fig. 1). At the time of admission, she was on treatment with diuretics, digoxin and acenocoumarol. There were no complaints of voice hoarseness, dysphagia or any other gastrointestinal symptoms. The hemogasanalysis was normal. An EKG showed atrial fibrillation. The trans-thoracic echocardiography (Table 1) revealed a mild decrease of systolic function at rest (ejection fraction of 46%), and moderate stenosis and regurgitation of the aortic valve, with mean and maximum gradients of 18.8 and 30.5 mmHg and a valve area of 0.97 cm. This examination also unexpectedly demonstrated a massively enlarged left atrium (LA), greater than the left and right ventricles, with a maximum diameter of 13 cm and a transverse diameter of 11.8 cm (104 cm) on the apical four-chamber view. Roughly calculating the atrium as a sphere, we reached a volume of 1 litre (Fig. 2). There was an associated moderate to severe regurgitation of the mitral valve prosthesis with a trans-prosthetic mean and maximum gradients of 8.45 and 19.28 mmHg, and a valve area of 1.08 cm. There was also evidence of dilated right-side heart sections, moderate tricuspidal regurgitation and pulmonary artery systolic pressure of 60 mmHg. Laboratory examinations revealed normal renal and liver functions with mild hyponatremia (132 mEq/L) and a mild iron deficiency anemia (Hb 11.6 mg/dl). No evidence of active rheumatic disease was documented. The ultrasound study of the abdomen showed congestive hepatomegaly. A diagnosis of decompensated heart failure syndrome (NYHA class III) was made, and oral treatment with high doses of furosemide, spironolactone and angiotensinreceptor blockers was initiated to manage the symptoms. During the hospitalization, because of the occurrence of bronchostenosis and leukocytosis, it was necessary to begin a course of treatment with steroids in infusion and an aerosol as well. After discharge, she was referred to the cardio-thoracic center of our hospital to evaluate the possibility of mitral valve prosthesis replacement. Left atrial enlargement is frequently found in clinical practice in a variety of heart conditions including rheumatic or non-rheumatic valvular heart disease, left ventricular diastolic dysfunction, hypertension, obesity, lone atrial fibrillation and left-to-right shunts [1]. Nevertheless, a giant LA is uncommon and defined according to the X-ray study appearance in which the LA forms the right border of the heart shadow and approximates the right chest with a cardio-thoracic ratio greater than 0.7; or as the atrium having at echocardiography an antero-posterior diameter larger than 8 cm. The normal LA is the most posterior chamber of the heart and is not located on the left, but in the middle of the chest. Therefore, when it enlarges, it moves rightward [2]. The Table 2 shows the literature review of the known causes of giant left atrium. This rare condition is more frequently seen in patients with mitral G. Parrinello D. Torres (&) S. Paterna M. Mezzero P. Di Pasquale C. Trapanese M. Cardillo G. Licata Biomedical Department of Internal and Specialist Medicine Policlinico ‘‘Paolo Giaccone’’, University Hospital of Palermo, Piazza Delle Cliniche 2, 90127 Palermo, Italy e-mail: daniele_torres@libero.it