Aurelio Caruso

Percutaneous mitral commissurotomy versus open mitral commissurotomy: a comparative study

OBJECTIVE Although many studies in medical literature are comparing percutaneous trans-septal mitral commissurotomy (PTMC) and open mitral commissurotomy (OMC), very few long-term comparative follow-ups are available. METHODS Between January 1991 and December 1997, 193 patients with isolated mitral stenosis were assigned either to PTMC (111 cases) or to OMC (82 cases). PTMC was performed in all cases with Inoue Ballon, OMC was performed with standard techniques. Categorical values were compared by chi square analysis, whereas continuous data were compared by Mann-Whitney test. Univariate survival and event free analysis (Kaplan-Meier+/-SE and log rank) were performed. Recurrent stenosis was classified any mitral valve area (MVA) less than 1.2 cm2 and whenever post-op. echo showed a loss more than 50% of the initial gain. Data were reported as mean+/-SD. Data concerning late echocardiographic assessment were studied with linear and logistic regression analysis. RESULTS The two groups were homogenous as far preoperative variables as sex, mean age, MVA, echo score and incidence of left atrial thrombosis were concerned. Mean NYHA was preoperatively higher in OMC (2.79+/-0.58) versus PTMC (2.42+/-0.5) (P = 0.001). There was no hospital mortality in both groups. Incidence of hospital complications was similar (4/ 111 after PTMC and 1/82 after OMC; P = 0.3). Seven year survival: 95.41+/-0.02 (PTMC) and 98.05+/-0.01 (OMC) (P = 0.3) and freedom from late complications did not show statistical differences: Embolism 98.78+/-0.01 in PTMC and 98.78+0.01 in OMC (P = 0.8); Recurrent stenosis 71.89+/-0.13 in PTMC versus 82.89+/-0.08 in OMC (P = 0.2); Reoperation 88.43+/-0.08 in PTMC versus 96.25+/-0.02 in OMC (P = 0.4). A larger MVA was found in patients undergone to OMC (2.05+/-0.35) versus PTMC (1.81+/-0.33) (P = 0.001). Furthermore mean NYHA was lower in OMC (1.14+/-0.3) versus PTMC (1.39+/-0.7) (P = 0.001). CONCLUSIONS Both techniques achieve with a low operative risk and low incidence of complications a good palliation of rheumatic mitral stenosis. Incidence of complications in the follow-up is similar. OMC allows a larger mitral valve area, a better functional recovery and a lower incidence of late mitral regurgitation.

Increased Epicardial Adipose Tissue Volume Correlates With Cardiac Sympathetic Denervation in Patients With Heart Failure

RATIONALE It has been reported that epicardial adipose tissue (EAT) may affect myocardial autonomic function. OBJECTIVE The aim of this study was to explore the relationship between EAT and cardiac sympathetic nerve activity in patients with heart failure. METHODS AND RESULTS In 110 patients with systolic heart failure, we evaluated the correlation between echocardiographic EAT thickness and cardiac adrenergic nerve activity assessed by (123)I-metaiodobenzylguanidine ((123)I-MIBG). The predictive value of EAT thickness on cardiac sympathetic denervation ((123)I-MIBG early and late heart:mediastinum ratio and single-photon emission computed tomography total defect score) was tested in a multivariate analysis. Furthermore, catecholamine levels, catecholamine biosynthetic enzymes, and sympathetic nerve fibers were measured in EAT and subcutaneous adipose tissue biopsies obtained from patients with heart failure who underwent cardiac surgery. EAT thickness correlated with (123)I-MIBG early and late heart:mediastinum ratio and single-photon emission computed tomography total defect score, but not with left ventricular ejection fraction. Moreover, EAT resulted as an independent predictor of (123)I-MIBG early and late heart:mediastinum ratio and single-photon emission computed tomography total defect score and showed a significant additive predictive value on (123)I-MIBG planar and single-photon emission computed tomography results over demographic and clinical data. Although no differences were found in sympathetic innervation between EAT and subcutaneous adipose tissue, EAT showed an enhanced adrenergic activity demonstrated by the increased catecholamine levels and expression of catecholamine biosynthetic enzymes. CONCLUSIONS This study provides the first evidence of a direct correlation between increased EAT thickness and cardiac sympathetic denervation in heart failure.

Prolapse of the “floppy” aortic valve as a cause of aortic regurgitation. A clinico-morphologic study

A clinico-pathologic study was performed in 25 patients undergoing aortic valve replacement because of regurgitation, caused by myxoid degeneration of the valve leaflets. Associated cardiac anomalies were floppy mitral valve (2 cases), floppy mitral valve and idiopathic hypertrophic subaortic stenosis (1), left atrial myxoma (1), and aortic coarctation at the isthmus (1). Three patients died (2 immediately and 1 on the 30th postoperative day). Pathological studies of the explanted valves showed deformities characterized by redundant thin leaflets which appeared soft and gelatinous. On histologic examination the fibrous layer of the leaflets was seen to be infiltrated by myxomatous tissue. Echocardiography showed the aortic root to be dilated in 13 patients and normal in the others. In those with normal aortic root, the histological examination of aortic wall disclosed minimal cystic medial necrosis in two cases. In contrast, more severe forms of cystic medial necrosis were evident in all patients having a dilated aortic root. Aortic valve replacement was performed in all cases. It was accompanied by a Bentall procedure (1 case), repair of ascending aorta dissection (2), replacement of the ascending aorta (1), mitral valve replacement (2), mitral valve replacement and apico-ascending aorta conduit (1) and excision of a left atrial myxoma (1). Our experience suggests that prolapse of the aortic valve due to floppy leaflets is a common degenerative disease which is generally associated with noninflammatory aortic root degeneration. This, together with aortic root dilatation, contributes to valve insufficiency. Nevertheless, the disease, when isolated (with normal aortic root), is liable in itself to produce aortic regurgitation. The need for early diagnosis is stressed, so as to be able to perform valve replacement.

Association of left ventricular hypertrophy and aortic dilation in patients with acute thoracic aortic dissection.

This study was designed to evaluate the impact of left ventricular mass on aortic diameters in patients who presented with acute thoracic aortic dissection where aortic dilation is common. Retrospective review of transthoracic and transesophageal echocardiograms was conducted for 63 patients treated for acute thoracic aortic dissection and for 16 normal subjects who were comparable for gender prevalence, age, heart rate, and blood pressure. The diameter of the aortic root was measured by transthoracic echocardiography. Diameters of the ascending aorta, and of the aorta at locations of 25, 30, and 35 cm from the dental arch were measured by transesophageal echocardiography. The findings indicated that all aortic diameters were significantly larger in patients with aortic dissection. Patients with aortic dissection also presented with greater left ventricular mass indices (p < 0.00001) than normal subjects. Fractional shortening and left atrial diameter measurements obtained in patients with aortic dissection were similar to those obtained in the control group. Overall, the left ventricular mass index exhibited univariate relationships with aortic root diameter (r= 0.27, p<0.02) and aortic diameters at 25 cm (r=0.51, p < 0.00001), 30 cm (r= 0.58, p < 0.00001), and 35 cm (r= 0.55, p < 0.00001) distal to the arch but not with the diameter of the ascending aorta. After adjusting for gender, body mass index, history of hyper tension and aortic dissection extent (Stanford types) by separate multivariate models, the authors found that the left ventricular mass index was independently associated with aortic diameters at 25 cm (β = 0.32, p < 0.001), 30 cm (β = 0.38, p < 0.0001), and 35 cm (β = 0.34, p < 0.0005) distal to the arch. They conclude that left ventricular mass is independently asso ciated with aortic arch and descending aorta diameters in patients with acute thoracic aortic dissection. Left ventricular hypertrophy may be considered a risk factor for aortic enlarge ment and subsequent dissection.

Aortic Dissection with Fistula to Left Atrium: Diagnosis by Transesophageal Echocardiography with Successful Repair

The aorta-atria fistula is an infrequent complication of aortic dissection, and it is rarely diagnosed before death. A 41-year-old man who 8 years previously had undergone prosthetic aortic valve replacement had an aortic dissection complicated by aorta-left atrial fistula. This patient had acute left heart failure associated with a systolic and diastolic murmur at the lower left sternal border suggesting an aortic prosthetic malfunction. The cardiac diagnosis was made with transesophageal echocardiography and Doppler color flow imaging; it was notable that the cardiac lesions were not detected by transthoracic echocardiography. On the basis of the echocardiographic findings, the patient underwent successful emergency replacement of the dissecting ascending aorta with closure of the aorta-left atrial fistula. Transesophageal echocardiography is the procedure of choice for defining this abnormality. In this case a prompt surgical repair consisting of replacement of the affected segment of the aorta with the prosthesis and closure of the fistula provided optimum resolution of the clinical situation.

Aortic Dissection with Fistula to Right Atrium After Heart Transplantation: Diagnosis by Transthoracic and Transesophageal Echocardiography

Aortic dissection with rupture into the right atrium is an extremely rare and rapidly fatal condition that may occur after cardiac surgery. We report the case of a 59‐year‐old woman with a 6‐year history of heart transplantation who presented with subacute illness characterized by chest pain and severe cardiac decompensation accompanied by a continuous murmur in the precordium. The diagnosis of aortic dissection complicated by right atrial fistula was made by the combination of transthoracic and transesophageal echocardiographic examination.

Device closure of 'complex' postinfarction ventricular septal defect.

Ventricular septal defect (VSD) is a life-threatening complication of acute myocardial infarction (MI), resulting in high mortality rate even in the case of a timely approach by surgical repair. Transcatheter closure is nowadays a reliable alternative to surgery, although currently deemed challenging or unsuitable in large and complex VSD. This article reports on a successful transcatheter approach in a critically ill patient with subacute right coronary-related, complex postinfarction VSD. In this patient, two sequentially deployed Amplatzer Septal Occluder devices stabilized the clinical conditions and hemodynamic parameters.

EPICARDIAL FAT TISSUE: A POTENTIAL ROLE IN AORTIC STENOSIS PATHOGENESIS

Epicardial adipose tissue (EAT) is widely accepted to be an active endocrine and paracrine organ that influences key pathogenic mechanisms of atherogenesis. Early atherosclerosis, cell proliferation, and calcifying phenotype are all hallmark features of aortic valve stenosis (AS). A potential

Pleuro-pericardiocenthesis: an unusual procedure

By echocardiography performed from the left posterior thoracic wall, we visualized a large posterior pericardial effusion and a left pleural effusion (Figs. 1 and 2). We inserted a catheter from the left posterior axillary line into the pleural (Fig. 1) and pericardial cavity (Fig. 2). A

Statin therapy modulates thickness and inflammatory profile of human epicardial adipose tissue

BACKGROUND Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation. METHODS Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies. RESULTS Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001). CONCLUSIONS The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.