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S Lentini

Publications and source records attributed to S Lentini.

At least 19 recordsLinked to original sources
PubMed2006

NT-pro-BNP in obstructive sleep apnea syndrome is decreased by nasal continuous positive airway pressure.

OBJECTIVE: The aim of this study was to evaluate the impact of obstructive sleep apnea syndrome (OSAS) on B-type natriuretic peptide (BNP) and to determine the effect of nasal continuous positive airway pressure (nCPAP) treatment on BNP levels. BACKGROUND: Increased sympathetic activity, repetitive rises in blood pressure, and apnea-induced wall stress may contribute as a trigger to release BNP in OSAS. However, there is uncertainty about whether OSAS affects BNP and whether application of nasal continuous positive airway pressure (nCPAP) ventilation affects release of BNP. PATIENTS AND METHODS: A prospective study in 69 consecutive patients with suspected sleep disordered breathing referred to our sleep laboratory was conducted. OSAS was confirmed in 26 normotensive and 34 hypertensive patients and ruled out in nine normotensive patients (controls) by polysomnography (PSG). RESULTS: Baseline N-terminal fragment of BNP prohormone (NT-pro-BNP) did not differ significantly between OSAS patients (hypertensive: mean +/-SEM 60.8+/-9.9 pg/ml, normotensive: 43.2+/-6.8 pg/ml) and controls (36.5+/-8.5 pg/ml). Application of CPAP resulted in a significant decrease of NT-pro-BNP in hypertensive (60.8+/-9.9 pg/ml to 47.6+/-7.4 pg/ml, p=0.023) and normotensive OSAS (43.2+/-6.8 pg/ml to 29.6+/-5.3 pg/ml, p=0.0002). In contrast, controls showed no significant differences in NT-pro-BNP after a second PSG (36.5+/-8.5 pg/ml to 40.7+/-12.3 pg/ml, p=0.597). CONCLUSIONS: Normotensive and hypertensive OSAS was not associated with a significant elevation of NT-pro-BNP. Application of nCPAP decreased NT-pro-BNP levels significantly in normotensive and, in particular, hypertensive OSAS. These findings may provide further evidence of the potential for nCPAP to improve cardiovascular comorbidity and co-mortality in OSAS and sleep disordered breathing, in general.

Continuous Positive Airway Pressure↗
PubMed2005

[Progressive upper lobe consolidation in a 73-year old healthy woman].

A 73-year old healthy woman presented for pacemaker replacement. Chest X-ray showed an right upper lobe consolidation. CT-scan and bronchoscopy with bronchoalveolar lavage could not yield a specific diagnosis. Due to progression of the consolidation in a CT scan after 10 weeks another bronchoscopy with transbronchial biopsy was performed and yielded bronchiolo-alveolar carcinoma. The patient underwent resection of the right upper lobe and middle lobe with curative intent.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2002

[Parvovirus B19 myocarditis in a young man with previous non-bacterial meningitis].

HISTORY AND CLINICAL FINDINGS: A 22-year old man presented with fatigue, dyspnea NYHA III and presyncopes that had persisted since a non-bacterial meningitis 3 months before. INVESTIGATIONS: Transthoracic echocardiography revealed a dilated left ventricle with an ejection fraction (EF) reduced to 35-40 % due to global hypokinesia. No pericardial effusion was seen; ECG and lung function test were normal. Serological, immunological and microbiological tests as well as nested PCR analysis of blood leucocytes for detection of cardiotropic pathogens were inconclusive. In endomyocardial biopsies retrieved from the left ventricular posterolateral wall, a chronic macro-phage-rich myocarditis was shown by histopathology and, in addition, Parvovirus B19 was identified as specific pathogen by use of nested PCR analysis. TREATMENT AND COURSE: At physical rest and with ACE inhibitor therapy (2.5 mg ramipril/day), heart failure decreased steadily. Follow-up echocardiography 1 month later revealed a left ventricle that was only slightly dilated with an EF of 50 %. 3 months later, the patient was markedly more load-bearing; the EF amounted to 55-60 %. CONCLUSIONS: Parvovirus B19 should be regarded as potential pathogen in case of suspected myocarditis in adulthood. Whether the previous non-bacterial meningitis was also attributable to this specific pathogen, remains open. Of note, however, the present case report by demonstrating a localized myocardial Parvovirus B19 infection without detectable systemic infection underscores the importance of molecular tests for diagnostic accuracy in manifest organ failure.

Adult↗
PubMed2002

[Noncompaction of the left ventricular myocardium. Case report and review of the literature].

Left ventricular non-compaction is an unclassified cardiomyopathy characterized by an excessively prominent trabecular meshwork due to an arrest in myocardial morphogenesis. We report on a 51-year-old female patient with abnormal myocardial trabeculations associated with a congenital mitral valve stenosis post commissurotomy at the age of 14. In the present case report, clinical manifestation of the disorder included impaired left ventricular systolic function and atrial fibrillation. Noncompaction was diagnosed by echocardiography and levocardiography. In addition, a review of the literature on this rare disorder is presented.

Adolescent↗
PubMed2002

[Chlamydia pneumoniae and cytomegalovirus in degenerative aortic valve stenoses].

Recent evidence suggests a causal relationship between inflammatory as well as infectious pathomechanisms and valvular degeneration. Based on the concept of chronic Chlamydia pneumoniae and cytomegalovirus (CMV) infections, and of variable stressors working on valvular microecology, the present study sought to assess the presence of the specific chlamydial heat shock protein (cHSP) 60, of CMV, of macrophages and of the human homologue hHSP60. Serial sections of high-grade degenerated native (n = 16) and prosthetic (n = 6) aortic valves were analyzed by immunohistochemistry for the presence of these determinants. Degenerated aortic valves revealed prevalence of Chlamydia pneumoniae in 41% (10 of 22) and CMV in 73% (16 of 22), while immunoreactive hHSP60 was present in 64% (14 of 22) and CD68 in 86% (19 of 22). Chlamydial HSP60, CMV and hHSP60 were predominantly found in valvular fibrosa; CMV showed a second predilection site at the ventricular luminal border. Both microorganisms revealed a strong correlation between each other (r = 0.73; p < 0.001) as well as with hHSP60 (cHSP60: r = 0.74; p < 0.001; CMV: r = 0.80; p < 0.001). Macrophage infiltration correlated with cHSP60 (r = 0.78; r < 0.001), CMV (r = 0.78; r < 0.001) and hHSP60 (r = 0.56; r = 0.007). Of note, the frequency of cHSP60, CMV and CD68 signaling was increased more than 5-fold in prosthetic valves compared to native valves (p = 0.017, p = 0.002 and p = 0.005). In summary, valvular infections of Chlamydia pneumoniae and of cytomegalovirus are frequently seen in degenerated aortic valves, irrespective of native or prosthetic origin. Colocalization of both HSP60 homologues and cytomegalovirus within macrophages in valvular fibrosa points to regional stressor effects that might be at least partly attributable to chronic persistent pathogen burden and molecular mimicry.

Aged↗
PubMed2001

[QT prolongation and torsade de pointes tachycardia during therapy with maprotiline. Differential diagnostic and therapeutic aspects].

HISTORY AND ADMISSION FINDINGS: A 69-year-old somnolent woman developed severe heart failure, aggravated by recurrent episodes of ventricular tachycardia. The patient showed central and peripheral edema. 24 hours earlier, she had suffered cerebral seizures that were successfully terminated by phenytoin. For 13 years, persistent atrial fibrillation had been frequency-controlled with antiarrhythmic drugs (verapamil and glycosides) and treated by oral anticoagulation. In addition, there had been long-term anti-depressant therapy with the tetracyclic agent maprotiline. INVESTIGATIONS: Torsade de pointes tachycardia was documented in the electrocardiograms. In addition, the QT interval was extensively prolonged (QTc = 0.70 sec). Neither electrolyte disturbances nor acute cardiac ischemia were seen. Echocardiography revealed a highly reduced ejection fraction of 25 % and a moderately dilated left ventricle. Angiography showed a collateralized occlusion of the right and plaques of the left coronary artery. TREATMENT AND COURSE: Repeated torsade de pointes tachycardia resulted in hemodynamic compromise and were terminated by defibrillations. After intravenous magnesium and xylocaine administration as well as with termination of maprotiline and antiarrhythmic co-medication, QT prolongation decreased. In addition, the recurrent torsade de pointes tachycardia stopped. Subsequently, however, there were several bradycardia episodes, QT duration remained long. Accordingly, a VVI pacemaker was implanted. Up to now, the patient is doing well. CONCLUSIONS: With antidepressant therapy, a risky constellation including comorbidity and interactions with potentially arrhythmogenic drugs may lead to QT prolongation. Medication that delays conduction or causes bradycardia may generally favour torsade de pointes tachycardia. In case of indispensable multi-drug therapy, regular clinical as well as electrocardiographic monitoring with special emphasis on QT interval is mandatory.

Aged↗
PubMed2001

[Epstein-Barr virus-associated pericarditis].

HISTORY AND ADMISSION FINDINGS: A 73 year old woman presented with increasing dyspnoea caused by a large pericardial effusion. INVESTIGATIONS: Transthoracic echocardiography revealed a diastolically 35 mm broad pericardial effusion. Subxiphoidal drainage controlled by ultrasound delivered 350 ml of a haemorrhagic fluid that was submitted to pathology and microbiology examination. This was completed by serological and immunological tests and a specific extensive search for malignant diseases, i. e. computer tomograms of chest and abdomen, mammography, bronchoscopy, gastroscopy and coloscopy. All examinations were negative. However, nested PCR analysis of blood leucocytes and of pericardial effusion revealed the pericardial presence of Epstein-Barr virus (EBV), consistent with a localized pericardial EBV persistence or reactivation. TREATMENT AND COURSE: Follow-up showed a complete resolution of the pericardial effusion without the necessity of further specific treatment. CONCLUSIONS: Although EBV infection is common in the general population, cardiac involvement, in particular in the adult, is infrequent and usually takes an uncomplicated course. The present case report demonstrates a beginning pericardial tamponade due to localized pericardial EBV persistence or reactivation without detectable systemic EBV infection. In addition, the importance of molecular tests for diagnostic accuracy is highlighted.

Aged↗
PubMed2001

[Decreased platelet aggregation during angiotensin-converting enzyme inhibitor therapy. Results of a pilot study].

BACKGROUND AND OBJECTIVE: Plaque rupture and subsequent thrombosis are key events in the complication and progression of atherosclerotic disease. Recently, the HOPE study showed a significant decrease in cardiovascular complications with the angiotensin converting enzyme (ACE) inhibitor (ramipril). To assess the therapeutic potential of this drug class, the present study evaluates the coagulative activity in cardiovascular patients with ACE inhibitors and compares these data with those of untreated patients and with those of patients taking aspirin, resp. METHODS: Blood samples from 204 patients with coronary heart disease and/or arterial hypertension were analyzed by whole-blood lumi-aggregometry. Platelet aggregation was determined by the increase in impedance across paired electrodes in response to the stimulatory agents collagen and ADP, respectively. The data were correlated with the presence or absence of ACE inhibitor and/or aspirin medication. Analogously, the coagulative potential of beta-blockers, calcium antagonists, CSE-inhibitors and nitrates were studied. RESULTS: As the central finding, study participants treated with ACE inhibitors showed a decreased platelet aggregation compared to untreated control patients, indicated by a significantly reduced increase in impedance. Platelet aggregation induced by collagen decreased by 18% (p = 0.025), that induced by ADP by 39% (p = 0.039). With aspirin medication, the collagen-induced decrease amounted to 20% (p = 0.020); no significant effect was seen by ADP stimulation. With combined intake of ACE inhibitors and aspirin, collagen-induced platelet aggregation was found markedly reduced. Platelet aggregation decreased by 26% (p = 0.003). Beta-blockers, calcium antagonists, CSE inhibitors and nitrates did not reveal a significant influence on platelet aggregation. CONCLUSIONS: ACE inhibition decreases platelet aggregation, as detected and quantified by ex vivo whole-blood aggregometry. Beyond known effects of this drug class, in particular on endothelium and fibrinolysis, antithrombotic effects may explain the positive influence on major clinical cardiovascular events.

Aged↗
PubMed1997

Beta 1 integrin is essential for teratoma growth and angiogenesis.

Teratomas are benign tumors that form after ectopic injection of embryonic stem (ES) cells into mice and contain derivatives of all primitive germ layers. To study the role of beta 1 integrin during teratoma formation, we compared teratomas induced by normal and beta1-null ES cells. Injection of normal ES cells gave rise to large teratomas. In contrast, beta 1-null ES cells either did not grow or formed small teratomas with an average weight of <5% of that of normal teratomas. Histological analysis of beta 1-null teratomas revealed the presence of various differentiated cells, however, a much lower number of host-derived stromal cells than in normal teratomas. Fibronectin, collagen I, and nidogen were expressed but, in contrast to normal teratomas, diffusely deposited in beta1-null teratomas. Basement membranes were present but with irregular shape and detached from the cell surface. Normal teratomas had large blood vessels with a smooth inner surface, containing both host- and ES cell-derived endothelial cells. In contrast, beta 1-null teratomas had small vessels that were loosely embedded into the connective tissue. Furthermore, endothelial cells were always of host-derived origin and formed blood vessels with an irregular inner surface. Although beta 1- deficient endothelial cells were absent in teratomas, beta 1-null ES cells could differentiate in vitro into endothelial cells. The formation of a complex vasculature, however, was significantly delayed and of poor quality in beta1-null embryoid bodies. Moreover, while vascular endothelial growth factor induced proliferation of endothelial cells as well as an extensive branching of blood vessels in normal embryoid bodies, it had no effect in beta 1-null embryoid bodies.

Animals↗
PubMed1996

Differentiation and integrity of cardiac muscle cells are impaired in the absence of beta 1 integrin.

Cellular interactions with substrata of the microenvironment are one of the major mechanisms for differentiation and morphogenesis. Many of these interactions are mediated via the beta 1 integrin subfamily of cell surface receptors, which are believed to transduce signals upon cell adhesion. We have used beta 1 integrin-deficient embryonic stem cells to test their ability to differentiate into cardiac muscle cells. We show here by several approaches that beta 1 integrin is important for normal cardiogenesis. First, the in vitro differentiation of beta 1 integrin-deficient embryonic stem cells into cardiac muscle cells is retarded. This is demonstrated by the delayed expression of cardiac muscle-specific genes and action potentials. Second, the specification of cardiac precursor cells into pacemaker-, atrial- and ventricular-like cells is significantly impaired in beta 1 integrin-deficient cells. The occurrence of atrial- and ventricular-like cells is reduced and transient. Only cells exhibiting peacemaker-like action potentials of high frequency and arrhythmias survive. Third, the sarcomeric architecture is incomplete and disarranged in the absence of beta 1 integrin. Fourth, beta 1-deficient embryonic stem cells can contribute to the developing heart in chimaeric mice but many areas with beta 1-null cells contain cell debris. The number of beta 1-null cells decrease from prenatal to postnatal stages and is lost completely in 6-month-old hearts. Thus, we conclude that interactions with the extracellular matrix via beta 1 integrin is necessary for differentiation and the maintenance of a specialized phenotype of cardiac muscle cells.

Animals↗
PubMed1995

Aortic valve replacement with pulmonary autograft in children and adults.

Aortic valve replacement with a conventional prosthesis is still flawed with complications, especially in children and young adults. Complex aortic root enlargement (Konno) is often needed because of small aortic diameter. The poor compliance with anticoagulation by teenagers and the risks associated with this made us look at alternative techniques. From November 1990 to June 1994, 70 patients were considered for pulmonary autografts in our institution; 64 underwent the procedure with one death and one failure to implant. Short-term results are excellent, with minimal gradient in 90% and minimal regurgitation in 96% of the patients. The long-term follow-up, hopefully, will confirm the superiority of this procedure over more conventional replacement.

Adolescent↗
PubMed1994

[Pulmonary autograft as aortic valve replacement in children].

The aortic stenosis represents 5% of all congenital cardiac pathology. The conventional treatments often do not give very satisfactory results. Since 1990, as alternative to the traditional aortic valve replacement, we used, in our institution, the Ross procedure (pulmonary autograft). This consists in using the pulmonary valve as an autograft in aortic position to replace the diseased valve. Then, the pulmonary outflow is reconstructed with a cryopreserved homograft. This study includes 15 patients, aged between 16 months and 18 years, treated with this technique since 1990. There has been no mortality. All the patients are alive at the follow-up, and all in NYHA functional class I. No reoperation has been necessary for valvular dysfunction. The post-operative doppler study at aortic level demonstrated those gradients: Mean + SD, 3.8 +/- 8.1 (range 0-23). No regurgitation haemodynamically important has been recorded at aortic level nor in the pulmonary position. Post-operative gradients at pulmonary level were: Mean + SD, 14.6 + 10.6 (range 14-32).

Adolescent↗
PubMed1994

Surgical treatment of left main coronary aneurysm.

Aneurysms of the coronary arteries occur in 0.3% to 4.9% of angiograms. Only 13 cases of left main artery (LMA) aneurysms have been reported. Of these, three were treated by ligation of the aneurysm and coronary revascularization; the others by revascularisation alone. We report the case of a 56 years old man presenting with unstable angina and previous history of myocardial infarction. Coronary angiography confirmed three vessels disease and the presence of an aneurysm of the LMA extending to the proximal part of the left anterior descending artery (LAD). The patient was treated with ligation of the aneurysm and total myocardial revascularization. The clinical and radiological features are reviewed, and the surgical options considered.

Angina, Unstable↗
PubMed1992

Emergency coronary artery surgery after refractory cardiac arrest: a single centre experience.

OBJECTIVE: To determine the incidence and outcome of refractory cardiac arrest necessitating emergency coronary artery bypass grafting. DESIGN: Retrospective survey of cardiac catheterisation and surgical records. SETTING: The London Chest Hospital. PATIENTS: All patients requiring emergency coronary artery bypass grafting after cardiovascular collapse in the catheterisation suite between January 1984 and December 1989. MAIN OUTCOME MEASURES: Incidence of refractory cardiac arrest in the study group and perioperative mortality. RESULTS: Thirteen of 8675 patients undergoing coronary arteriography or angioplasty had refractory cardiac arrests. Five patients died, but the remainder survived to be discharged from hospital without serious morbidity. CONCLUSION: Without immediate surgical intervention the mortality for these 13 patients would have been 100%.

Aged↗
PubMed1980

Clinical trial of xipamide in the treatment of hypertension.

Nine patients with hypertension were given xipamide 40 mg orally as monotherapy on alternate days. An additional seventeen patients had xipamide added to an existing treatment regime of clonidine 450 micrograms per day. Xipamide alone produced a significant fall in blood pressure comparable to that obtained with clonidine alone. However, a significant further reduction was obtained when xipamide was added to the existing clonidine regime.

Administration, Oral↗