Anterior Mitral Valve Aneurysm Is an Uncommon Complication of Aortic Valve Infective Endocarditis: A Case Report.

BACKGROUND Mitral valve aneurysms (MVAs) are uncommon conditions frequently associated with aortic valve endocarditis. They may be complicated by perforation and severe mitral regurgitation (MR). Optimal treatment of MVA, and in particular the best timing for surgery, are uncertain. CASE REPORT A 62-year-old man with a recent history of dental surgery presented to the Emergency Department complaining relapsing fever. A first echocardiogram demonstrated infective endocarditis of the aortic valve. The patient was primarily managed with specific antibiotic therapy. Despite this, a few days later he suffered from splenic embolization and an MVA with MR was detected. Surgical replacement of the mitral and aortic valves was therefore performed. CONCLUSIONS MVAs are infrequent but potentially severe complications of AV endocarditis. In the absence of definite treatment indication, the correct time for surgery should depend on concomitant clinical and infective features.

Sudden death after valve-in-valve procedure due to delayed coronary obstruction: a case report.

BACKGROUND: Valve-in-valve transcatheter aortic valve implantation for degenerated aortic bioprostheses is an effective option for patients at high risk for redo surgery, even if it may be burdened by complications more common in specific settings, such as, coronary artery obstruction. CASE PRESENTATION: We present the case of a Caucasic 84-year-old woman with degeneration of a previously implanted aortic Mitroflow bioprosthesis. She underwent a valve-in-valve transcatheter aortic valve implantation with a CoreValve® bioprosthesis. End-procedure coronary angiography demonstrated maintained perfusion of both coronary arteries. However, few hours later, she experienced sudden cardiac death. An autopsy showed that Mitroflow prosthesis leaflets were higher than the left main coronary ostium, and no other possible cause for the sudden death. Fatality was thus ascribed to left main coronary ostium obstruction due to apposition of the Mitroflow leaflet pushed upward by the late expansion of CoreValve®. CONCLUSIONS: Coronary artery obstruction is a frequently fatal complication which usually presents just after valve implantation, but, as reported in our case, it may also have a delayed presentation. Accurate patient's selection and intraoperative preventive measures can reduce this eventuality.

One-year GH replacement therapy reduces early cardiac target organ damage (TOD) in adult GHD patients.

Hypopituitarism reduces life expectancy and increases the risk of cardiovascular and cerebrovascular diseases, as well as death. Abnormalities in the cardiovascular system may be independently related to GH deficiency (GHD). The aim of this study was to prospectively investigate coronary flow reserve and diastolic function in GHD adult patients at diagnosis and after 1 year of GH replacement therapy. As control group, an age- and sex-matched population was chosen. All patients and controls were non-smokers, non-diabetic, and normotensive, with no history of vascular disease. 14 patients with adult-onset GHD and 17 controls represent the two study groups. Anthropometric data, blood pressure, lipid profile, glycosylated hemoglobin (HbA1c) and IGF-I plasma levels, coronary flow reserve (CFR), and LV diastolic function (evaluated by E/A) were collected in all subjects before and after 12 months of GH replacement therapy. Compared with controls, systolic and diastolic blood pressure and LDL cholesterol levels were significantly higher at baseline and return, comparable to controls after 1 year of GH replacement (GHRT). GHD patients showed a blunted CFR at baseline (P < 0.001) and a significant improvement after GHRT, returning to values comparable with those recorded in the control group. In addition, after therapy a significant (P < 0.001) improvement in E/A was recorded. One year of GH therapy improves CFR and E/A in the patient population analyzed, thereby encouraging the early start of GHRT.

Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes.

BACKGROUND: Chronic cardiotoxicity is less common in male than in female patients receiving doxorubicin and other anthracyclines at puberty and adolescence. We hypothesized that this sex difference might be secondary to distinct activities of sex hormones on cardiomyocyte senescence, which is thought to be central to the development of long-term anthracycline cardiomyopathy. METHODS AND RESULTS: H9c2 cells and neonatal mouse cardiomyocytes were exposed to doxorubicin with or without prior incubation with testosterone or 17ß-estradiol, the main androgen and estrogen, respectively. Testosterone, but not 17ß-estradiol, counteracted doxorubicin-elicited senescence. Downregulation of telomere binding factor 2, which has been pinpointed previously as being pivotal to doxorubicin-induced senescence, was also prevented by testosterone, as were p53 phosphorylation and accumulation. Pretreatment with the androgen receptor antagonist flutamide, the phosphatidylinositol 3 kinase inhibitor LY294002, and the nitric oxide synthase inhibitor L-NG-nitroarginine methyl ester abrogated the reduction in senescence and the normalization of telomere binding factor 2 levels attained by testosterone. Consistently, testosterone enhanced the phosphorylation of AKT and nitric oxide synthase 3. In H9c2 cells, doxorubicin-stimulated senescence was still observed up to 21 days after treatment and increased further when cells were rechallenged with doxorubicin 14 days after the first exposure to mimic the schedule of anthracycline-containing chemotherapy. Remarkably, these effects were also inhibited by testosterone. CONCLUSIONS: Testosterone protects cardiomyocytes against senescence caused by doxorubicin at least in part by modulating telomere binding factor 2 via a pathway involving the androgen receptor, phosphatidylinositol 3 kinase, AKT, and nitric oxide synthase 3. This is a potential mechanism by which pubescent and adolescent boys are less prone to chronic anthracycline cardiotoxicity than girls.

[Postoperative atrial fibrillation in noncardiac thoracic surgery]. / Fibrillazione atriale postoperatoria nella chirurgia toracica non cardiaca.

Atrial fibrillation is the most common arrhythmia in clinical practice. Although postoperative atrial fibrillation occurs in a small percentage of the total number of cases, it is associated with increased mortality, longer hospital stay and higher hospitalization costs, making this issue of particular relevance. The aim of this literature review is to describe the risk profile of this patient subset and to focus on the current knowledge of available prophylactic and therapeutic strategies.

Functional tricuspid regurgitation: an underestimated issue.

This review article focuses on functional tricuspid regurgitation (FTR) that has long been a neglected and underestimated entity. FTR is defined as leakage of the tricuspid valve during systole in the presence of structurally normal leaflets and chordae. FTR may be secondary to several heart diseases, more commonly mitral valve disease, pulmonary hypertension, atrial fibrillation, cardiomyopathies, right ventricular dysplasia, and idiopathic annular dilatation. The reported prevalence of moderate or greater FTR is roughly 16%, but it rises up to 89% when considering FTR of any grade. According to the recommendations of the European Association of Echocardiography, two-dimensional transthoracic echocardiography (TTE) is the first-line imaging modality for the assessment of valvular regurgitation, whereas three-dimensional TTE may provide additional information in patients with complex valve lesions. Transesophageal echocardiography may be used when TTE results are inconclusive. The natural history of FTR is unfavorable, even in less than severe tricuspid regurgitation. Data from the literature suggest that moderate or greater FTR is a risk factor for worse survival. In addition, FTR of any grade may worsen over time, which makes it reasonable to consider the correction of FTR at an early stage, preferably at the time of mitral valve surgery. Tricuspid valve annuloplasty is the gold standard surgical treatment for FTR and is associated with a recurrence rate, defined as postoperative moderate or severe FTR, ranging from 2.5 to 5.5% at 1-year follow-up.

Iatrogenic left main coronary ostial stenosis after a Bentall procedure in an asymptomatic young man.

Coronary ostial stenosis is a rare but potentially fatal sequela of aortic surgery. The clinical presentation can include acute coronary syndromes, ventricular arrhythmias, congestive heart failure, or sudden death. Herein, we present what we believe is the first reported case of asymptomatic iatrogenic left main coronary ostial stenosis. The patient was an active 34-year-old man who had undergone a modified Bentall procedure and was asymptomatic thereafter. Seven months after that operation, exercise stress testing showed electrocardiographic signs of asymptomatic myocardial ischemia at high workload, and coronary angiography revealed severe nonatherosclerotic left main ostial stenosis. Percutaneous coronary intervention and stenting of the unprotected left main stenosis was successful, and patency at 8 months was apparent on coronary angiography.The conventional treatment for coronary ostial stenosis, coronary artery bypass grafting, carries a high risk of perioperative infarction, morbidity, and death. We found that percutaneous coronary intervention with stenting yielded positive short- and long-term results and may provide an alternative to cardiac surgery in these high-risk patients. We recommend that physicians evaluate even asymptomatic patients for left main coronary ostial stenosis after aortic surgery so that early diagnosis and treatment can avert severe clinical manifestations.

Combined use of urinary neutrophil gelatinase-associated lipocalin (uNGAL) and albumin as markers of early cardiac damage in primary hypertension.

BACKGROUND: Neutrophil Gelatinase-Associated Lipocalin (NGAL) is an early and specific marker of acute kidney dysfunction. Recent evidences suggest that NGAL may also be involved in chronic vascular remodeling during the development of atherosclerosis. Albuminuria, a powerful predictor of cardiovascular events, is thought to reflect widespread subclinical vascular abnormalities. We investigated the relationship between urinary NGAL (uNGAL), albuminuria and left ventricular mass (LVM) in patients with primary hypertension. METHODS: A total of 120 untreated, non diabetic patients with primary hypertension (mean age 47 ± 9 years) were studied. uNGAL was measured by a chemiluminescent microparticle method, optimized on a fully automated analytical platform (ARCHITECT, Abbott Diagnostics Inc, Rome, IT). Albuminuria was measured by immunonephelometry on an Immage Immunochemistry System (Beckman Coulter, Inc., Fullerton, California, USA) and expressed as albumin/creatinine ratio (ACR). LVM was assessed by echocardiography and indexed to body surface area (LVM/BSA). RESULTS: No significant correlation was found between uNGAL and ACR; however, both variables were directly related to clinic systolic blood pressure (rho=0.241, p=0.0085 and rho=0.248, p=0.0068 respectively), left ventricular relative wall thickness (rho=0.251, p=0.0156 and rho=0.263, p=0.0013 respectively), and LVM/BSA (rho=0.285, p=0.0062 and rho=0.213, p=0.0410 respectively). The uNGAL and ACR simultaneous increase above their respective median values was associated with higher LVM/BSA values (p=0.0109) and with a higher prevalence of left ventricular hypertrophy (LVH) (p=0.0017). Furthermore, logistic regression analysis showed that the risk of presenting LVH increased more than 4-fold when uNGAL and ACR were both above the median value, even after adjustment for age, gender and blood pressure values. CONCLUSIONS: The simultaneous increase in uNGAL and ACR excretion is significantly associated with the increase of LVM in low risk patients with primary hypertension. This association is clinically significant for the early assessment of cardiac damage in hypertension.

Guide wire fracture during percutaneous transluminal coronary angioplasty: possible causes and management.

A 46-year-old woman underwent diagnostic coronary angiography in our institution due to a myocardial ischemia following a dobutamine echo-stress test. The patient showed critical stenosis of the left anterior descending (LAD) artery involving the ostium of a large diagonal branch. The planned treatment of coronary bifurcation by percutaneous coronary intervention (PCI) was direct stenting of the main branch with 'jailed' wire technique to protect the side branch, provisional T stenting of the side branch, and final kissing balloon inflation. After successful stent implantation in the LAD, the 'jailed' wire fractured during withdrawal: the distal part of the fragment was trapped in the side branch, and the proximal one was knotted in the LAD, left main coronary and the aortic bulb. We decided not to retrieve the fragment by snare, and we planned heart surgery to safely retrieve the fragment and bypass the side branch not treated by percutaneous coronary interventions. Angiographic control nine months after surgery showed non in-stent restenosis; patient is alive and event-free at 18 months' clinical follow-up. In conclusion, percutaneous management of particularly complex bifurcational lesions may be associated with procedural risks; accordingly, it is important to consider and be ready for a rescue surgical revascularization.

Left main coronary stenosis as a consequence of bentall operation: percutaneous treatment.

A 65-year-old man suffering from ascending aorta aneurysm and atherosclerotic three vessel disease without left main involvement underwent aortic root replacement with coronary ostia reimplantation according to the modified Bentall technique and multiple coronary artery bypass grafts. Gelatin-resorcin-formaldehyde glue was used to reinforce the aortic coronary buttons and to facilitate hemostasis. Five months after surgery, the patient experienced rapidly worsening effort angina. Coronary angiography showed severe left main narrowing. The considerable amount of time that elapsed between surgery and the onset of symptoms implies that the problem was not related to an imperfect suture technique, but was most likely caused by an inflammatory and proliferative response to the glue that had been used. We performed elective percutaneous coronary intervention and stenting of the protected coronary vessel without technical difficulties and with a satisfactory final result. The patient is currently symptom-free after 1 year's follow-up.

Percutaneous closure of patent foramen ovale in patients with presumed paradoxical embolism: periprocedural results and midterm risk of recurrent neurologic events.

OBJECTIVE: To report our data on selected patients with previous paradoxical embolism who underwent transcatheter patent foramen ovale (PFO) closure. METHODS: Between July 2001 and July 2007, percutaneous PFO closure was performed on 128 patients (65 women, mean age: 46 +/- 12.8 years). Patent foramen ovale closure was recommended for secondary prevention in patients with previous transient ischemic attacks (52.5%), stroke (46%), or peripheral embolism (1.5%). RESULTS: Implantation was successful in all patients, and at the end of intervention, complete PFO closure was achieved in 70.3% of them. There were no "major" complications (ie, deaths, device embolization or thrombosis, need for cardiac surgery). The overall incidence of complications (mostly hemorrhagic) was 7%. The mean follow-up period was 32 months. Complete closure had been achieved in 78.4% and in 82.5% of patients at the third month of transesophageal echocardiography examination and at the sixth month of transcranial Doppler examination, respectively. There were no recurrent thromboembolic events during the follow-up period. CONCLUSIONS: Percutaneous closure of PFO is a feasible procedure, but it is not a risk-free technique. However, in correctly selected patients (ie, large PFO and those at risk for neurologic relapse), nearly complete PFO closure seems to provide protection from future neurologic ischaemic events at midterm follow-up.

Biliopancreatic diversion reduces QT interval and dispersion in severely obese patients.

OBJECTIVES: The objectives were to evaluate QT interval (QTc) and QT-interval dispersion (QTd) in severely obese individuals and to determine the effects of biliopancreatic diversion (BPD) and weight loss after BPD on ventricular repolarization parameters. BACKGROUND: People with severe obesity (SO) have a 50% to 100% increased risk of death associated with a 1.6-fold increased risk of sudden death. BPD surgery induces rapid and considerable weight loss through severe lipid malabsorption, thus achieving long-term weight control. RESEARCH METHODS AND PROCEDURES: A total of 85 subjects with SO (age, 42 +/- 12 years; 66 females; mean body weight, 120 +/- 29 kg; BMI, 45 +/- 11 kg/m(2)) of 330 who had a bariatric surgical consultation between January 2001 and July 2002 were enrolled. Inclusion criteria were sinus rhythm, unremarkable 12 leads surface electrocardiogram, no atrioventricular blocks and/or bundle branch blocks, normal serum electrolyte profile, and no medical therapies exerting known effects on QTc. Exclusion criteria were previous diagnosis of coronary artery disease, known cardiovascular disease, atrial fibrillation or any other known cardiac arrhythmias, cancer, or renal dysfunction. RESULTS: A total of 86% of patients had QTc >440 ms and/or QTd >60 ms. Subjects with SO showed a mean maximum QTc of 446 +/- 28 ms and a mean QTd of 52 +/- 20 ms. A close correlation was found between QTc and QTd (p < 0.0001; R(2) = 0.33). One month after BPD, mean QTc was 420 ms and remained stable at follow-up; QTd was 32 ms at 1 and 6 months and became 35 ms at 1 year. CONCLUSIONS: Ventricular repolarization abnormalities are significantly increased in subjects with SO. Reduction of QT abnormalities after BPD is independent of weight loss and is caused by the 100% reduction of glucose plasma shortly after surgery. This effect may be related to surgical interruption of the entero-insular axis.

Optimizing global risk evaluation in primary hypertension: the role of microalbuminuria and cardiovascular ultrasonography.

OBJECTIVE: To assess the impact and cost-effectiveness of microalbuminuria and cardiovascular ultrasonography in evaluating the risk profile in primary hypertension. METHODS: Four hundred and five untreated patients with primary hypertension underwent a routine, traditional work-up plus evaluation of albuminuria and ultrasound (US) assessment of cardiac and vascular structures. Albuminuria was measured as the albumin to creatinine ratio in three non-consecutive first-morning urine samples. Left ventricular mass index was assessed by MB-mode echocardiography and carotid intima-media thickness by high-resolution US scan. The impact of these tests on patient risk classes, as indicated by European Society of Hypertension-European Society of Cardiology (ESH-ESC) guidelines, was assessed with respect to their cost and sensitivity. RESULTS: The prevalence of microalbuminuria, left ventricular hypertrophy and carotid intima-media thickening or carotid plaque was 13, 49 and 32%, respectively. The combined use of albuminuria, cardiac and vascular ultrasonography led to the detection of a significantly higher percentage of patients at high/very high risk. The three tests differ in sensitivity (albuminuria, 20%; echocardiography, 65%; and carotid ultrasound, 41%). The signs of target organ damage (TOD) only partly cluster within the same subgroup of patients and, thus, all three tests should be performed in order to maximize the sensitivity of the evaluation process. The diagnostic algorithm yielding the lowest cost per detected case of TOD is the search for microalbuminuria followed by cardiac and carotid ultrasound assessment. CONCLUSIONS: Ultrasonographic detection of TOD is a sensitive tool in the identification of high-risk patients, but should be preceded by a routine search for microalbuminuria in order to optimize the cost-effectiveness of the diagnostic work-up.

Mild renal dysfunction and subclinical cardiovascular damage in primary hypertension.

The presence of mild renal dysfunction is associated with high cardiovascular morbidity and mortality rates in patients with primary hypertension. The pathophysiological mechanisms underlying this association are currently unknown. We investigated the relation between mild renal dysfunction and subclinical cardiovascular organ damage in 358 never previously treated patients with primary hypertension. Mild renal dysfunction was defined as a creatinine clearance <60 mL/min and/or the presence of microalbuminuria. Left ventricular mass index and carotid intima-media thickness were assessed by ultrasound scan. The prevalence of mild renal dysfunction, left ventricular hypertrophy, and carotid plaque was 18%, 48%, and 28%, respectively. Mild renal dysfunction was related to the presence of several risk factors, such as older age, higher blood pressure levels and lipid status, and smoking habits. Patients with the highest left ventricular mass and carotid intima-media thickness (upper quartiles) showed a higher prevalence of mild renal dysfunction (P<0.0001). After adjusting for duration of hypertension, mean blood pressure, smoking habits, and age, we found that the risk of left ventricular hypertrophy and/or carotid atherosclerosis increased by 43% with each SD reduction in creatinine clearance, and by 89% with each SD increase in albuminuria. Mild renal dysfunction is associated with preclinical end-organ damage in patients with primary hypertension. These data may help explain the high cardiovascular mortality rates reported in patients with low glomerular filtration rate or with increased albuminuria. The evaluation of creatinine clearance and urinary albumin excretion could be useful for identifying subjects at higher cardiovascular risk.