Caterina Trapanese

A new option in measuring bioimpedance in congestive heart failure

To the Editor: We read with particular attention the interesting article of Tang and Tong concerning the measurement of impedance for assessing volume status in heart failure (HF). This technology is useful in detecting subclinical congestion and predicting future HF events. However, the authors have focused their attention only on central fluid overload. To this proposal, we would briefly discuss about a new promising method, not mentioned in the critical review, able to measure whole-body overload. The bioelectrical impedance analysis (BIA) is a reproducible, inexpensive, patient-bed method used specifically to assess with high accuracy hydration state in heart diseases and in other illness. Recently, the international literature have focused their concentration on this emerging diagnostic tool for its simplicity, rapidity, noninvasiveness, ability to detect whole-body fluid accumulation, and work operability independent from mathematical models using only raw data: a combination of resistance (Rz) and reactance (Xc). In the standard whole-body tetrapolar BIA, electrodes were on the dorsum of the hand and on the dorsum of the foot of the right side. According to the R-Xc graph method of vector BIA by Piccoli et al, the impedance measurement, standardized for the height, establishes rapidly the systemic hydration state. This new methodological approach is particularly valuable in acute and also chronic HF where comparisons of direct impedance measurements of a patient with reference values are more useful than equations predicting average body compartments that are influenced by sampling error of regression coefficients, race, and diseases. Moreover, BIA, contrary to the band electrode method or implanted device-based method, is not limited by the presence of some comorbidity (renal failure and liver diseases) and is not to be implanted because it is simply applicable at the patients bed. Paterna et al used BIA safely in monitoring hospitalized patients with refractory congestive HF treated with high-dose intravenous furosemide and hypertonic saline solutions. Castillo Martínez et al demonstrated, instead, the cross-inverse correlation between the fluid overload estimated with BIA and New York Heart Association functional class. Our team has validated this tool in differentiating acute dyspnea due to HF in emergency room; in that work, it was demonstrated as the crossinverse correlation of BIA measures with B-type natriuretic peptide levels. Furthermore, we also demonstrated the utility of BIA in monitoring body hydration in exerciser patients with compensated congestive HF. In conclusion, BIA is a suitable technique in clinical practice for detecting not only pulmonary but also wholebody fluid overload. A concealed or bad-assessed systemic fluid accumulation is a crucial joint in HF management, which frequently remains undiagnosed or not appropriately treated, determining recurrent hospital readmission and disease progression. For these reasons, BIA represents, in our mind, the present and the future of HF assessment and needs more careful consideration and research efforts.

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.

Sudden severe abdominal pain after a single low dose of paracetamol/codein in a cholecystectomized patient: learning from a case report.

We report the case of an elderly patient with diastolic heart failure and renal insufficiency admitted to hospital as he complained of having a history of hypogastric pain and dysuria without fever due to renal lithiasis and urinary infection. Because the pain was persistence, and considering the presence of renal dysfunction, it was administered a single low dose of paracetamol/codein (500/30 mg). After about 1 hour of the administration, he suddenly complained of the onset of a lancinating epigastric pain radiating to the whole abdomen and retrosternum accompanied by nausea. The electrocardiogram (EKG) was negative for myocardial infarction and computed tomography excluded aortic dissection and other causes of acute abdomen. Laboratory tests showed instead liver and pancreatic damage. The symptomatology was relieved 3 hours later of the onset after antispastic treatment with anticholinergics (floroglucine). The likely underlying pathophysiological mechanism is the codein-induced spasm of the sphincter of Oddi combined with dysfunction of the same sphincter and reduced bile storage capacity related to a previous cholecystectomy. When a similar event does not regress, it may lead to more severe conditions such as acute pancreatitis. Since codein is a widely used drug, this report may suggest cholecystectomy as a contraindication during administration for the risk of occurrence of these complications.

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.

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

NON-INVASIVE DETECTION OF PCWP IN DECOMPENSATED HEART FAILURE PATIENTS TREATED WITH INTRAVENOUS HIGH-DOSE FUROSEMIDE AND SMALL-VOLUME HYPERTONIC SALINE SOLUTION: RELATIONSHIP WITH BNP AND BIOIMPEDANCE

Background: Decompansated heart failure (DHF) is a broad of spectrum of signs and symptoms characterized by fluid’s accumulation in the interstitial space of the lungs and whole body. We evaluate the non-invasive detection of pulmonary capillary wedge pressure (PCWP) by Tissue Doppler Analysis DHF patients underwent treatment with intravenous high-dose furosemide and small-volume hypertonic saline solution (HSS). Moreover we investigate its relationship with changes of BNP plasma levels and Whole-body (WB) and segmental (Seg) bioelectrical impedance analysis (BIA), a non-invasive tool useful to estimate the hydration status and fluid distribution. Methods and Results: 66 consecutive patients (63 to 82 yr, 43 men) admitted for DHF (EF<45%, NYHA class III-IV) underwent tailored therapy with intravenous furosemide and HSS were enrolled. 22 patients with compensated left ventricular dysfunction and 22 healthy subjects were considered as controls. WB and Seg BIA parameters were drawn at hospital entry and after clinical stabilization with treatment. At discharge there was a significant reduction of PCWP (-7 mmHg, p<.001) as BNP levels (p<.001) and significant increase of BIA parameters (p<.001) in DHF patients. Furthermore significant correlations of PCWP with BNP serum levels (p<.001) and BIA parameters (p<.001) and of BNP levels and BIA parameters (p<.001) at baseline and at clinical stabilization correlation were found. Conclusion: our data suggest that non-invasive evaluation of PCWP is a valuable and useful way in management of DHF. Moreover it is related to neuro-hormonal activation and whole-body and pulmonary fluid accumulation in these patients. High-dose of intravenous furosemide plus HSS are well tolerated and improve the in-hospital outcome with an effective hemodynamic stabilization, the normalization of hydration status and a positive neuro-hormonal modulation.