PubMed Health⌕ Search

Biomedical subjects

P Asseman

Publications and source records attributed to P Asseman.

At least 19 recordsLinked to original sources
PubMed2006

[Tako-tsubo syndrome and left ventricular obstruction: report of one case].

We report here the case of an 80 year old female suffering from Tako-tsubo syndrome diagnosed following type B aortic dissection, treated surgically with an aortic endoprosthesis. The recovery was marked by the secondary development of left intraventricular obstruction. Regression of the electrical and ultrasound anomalies was slow, taking 4 months of treatment with a beta-blocker. The intraventricular obstruction seemed to occupy a central role in this case, and we discuss the significance of this mechanical phenomenon in the pathophysiology of this syndrome.

Adrenergic beta-Antagonists↗
PubMed2006

Functional mitral regurgitation and chronic heart failure.

Functional mitral regurgitation (MR) frequently develops during the progression of chronic heart failure and predicts poor outcome. Impaired left ventricular (LV) function, LV remodeling associated with papillary muscle apical displacement and annular enlargement result in decreased mitral closing forces and tenting of the mitral valve at closure. Reduced closing forces and tenting both promote MR. Active myocardial ischemia, myocardial asynchronism and excessive loading conditions worsen MR at rest and during exercise. The therapeutic target in functional MR is the left ventricle and not the valve.

Adrenergic beta-Antagonists↗
PubMed2005

Cardiac resynchronisation therapy reduces functional mitral regurgitation during dynamic exercise in patients with chronic heart failure: an acute echocardiographic study.

OBJECTIVES: To assess non-invasively the acute effects of cardiac resynchronisation therapy (CRT) on functional mitral regurgitation (MR) at rest and during dynamic exercise. METHODS: 21 patients with left ventricular (LV) systolic dysfunction and functional MR at rest, treated with CRT, were studied. Each patient performed a symptom-limited maximal exercise with continuous two dimensional Doppler echocardiography twice. The first exercise was performed with CRT; the second exercise was performed without CRT. Mitral regurgitant flow volume (RV), effective regurgitant orifice area (ERO) and LV dP/dt were measured at rest and at peak exercise. RESULTS: CRT mildly reduced resting mitral ERO (mean 8 (SEM 2) v 11 (2) mm(2) without CRT, p = 0.02) and RV (13 (3) v 18 (3) ml without CRT, p = 0.03). CRT attenuated the spontaneous increase in mitral ERO and RV during exercise (1 (1) v 9 (2) mm(2), p = 0.004 and 1 (1) v 8 (2) ml, p = 0.004, respectively). CRT also significantly increased exercise-induced changes in LV dP/dt (140 (46) v 479 (112) mm Hg/s, p < 0.001). CONCLUSION: Attenuation of functional MR, induced by an increase in LV contractility during dynamic exercise, may contribute to the beneficial clinical outcome of CRT in patients with chronic heart failure and LV asynchrony.

Aged↗
PubMed1999

Free-floating thrombi in the right heart: diagnosis, management, and prognostic indexes in 38 consecutive patients.

BACKGROUND: Floating right heart thrombi (FRHTS) are a rare phenomenon, encountered almost exclusively in patients with suspected or proven pulmonary embolism and diagnosed by transthoracic echocardiography. Their management remains controversial. METHODS AND RESULTS: We report on a series of 38 consecutive patients encountered over the past 12 years. Thirty-two patients were in NYHA class IV, 20 in cardiogenic shock. Echocardiography usually demonstrated signs of cor pulmonale: right ventricular overload (91.7% of the population), paradoxical interventricular septal motion (75%), and pulmonary hypertension (86. 1%). The thrombus was typically wormlike (36 of 38 patients). It extended from the left atrium through a patent foramen ovale in 4 patients. Pulmonary embolism was confirmed in all but 1. Mortality was high (17 of 38 patients) irrespective of the therapeutic option chosen: surgery (8 of 17), thrombolytics (2 of 9), heparin (5 of 8), or interventional percutaneous techniques (2 of 4). The in-hospital mortality rate was significantly linked with the occurrence of cardiac arrest. Conversely, the outcome after discharge was usually good, because 18 of 21 patients were still alive 47.2 months later (range, 1 to 70 months). CONCLUSIONS: Severe pulmonary embolism was the rule in our series of FRHTS (mortality rate, 44.7%). The choice of therapy had no effect on mortality. Emergency surgery is usually advocated. However, thrombolysis is a faster, readily available treatment and seems promising either as the only treatment or as a bridge to surgery. In patients with contraindications to surgery or lytic therapy, interventional techniques may be proposed.

Adult↗
PubMed1999

[Pheochromocytoma simulating myocardial infarct. Apropos of a case].

The authors report the case of a pheochromocytoma in a 67 year old man in whom the initial clinical presentation suggested myocardial infarction. Pheochromocytoma is usually an adrenal tumour with a very variable clinical symptomatology. It is very rare for cardiac disease to be a presenting symptom. The diagnosis was suggested by major blood pressure abnormalities occurring after starting medical treatment for infarction. Pheochromocytomas may cause serious cardiovascular disorders. The diagnosis must be suspected in the presence of atypical signs, an essential requirement to reduce the mortality of the disease.

Adrenal Gland Neoplasms↗
PubMed1998

Enhanced monocyte tissue factor response after experimental balloon angioplasty in hypercholesterolemic rabbit: inhibition with dietary L-arginine.

BACKGROUND: There is evidence that tissue factor (TF) is a major contributor to the thrombogenicity of a ruptured atherosclerotic plaque. Nitric oxide (NO) has antiatherogenic and antithrombotic properties. We investigated whether L-arginine (L-arg), the endogenous precursor of NO, might affect the ability of monocytes to produce TF. METHODS AND RESULTS: We studied TF expression in 18 rabbits with atherosclerosis induced by bilateral iliac damage and 10 weeks of a 2% cholesterol diet. Six weeks after the initiation of the diet, an angioplasty was performed. After angioplasty, the surviving rabbits (n=15) were randomized to receive L-arg (2.25%) supplementation in drinking water (L-arg group, n=8) or no treatment (untreated group, n=7). TF expression was evaluated in mononuclear cells from arterial blood in the presence and absence of endotoxin stimulation. Monocyte TF expression, as assessed with an amidolytic assay, did not differ significantly before or after the induction of atherosclerotic lesions (87+/-15 versus 70+/-12 mU of TF/1000 monocytes, P=NS). Endotoxin-stimulated TF activity increased significantly 4 weeks after angioplasty (138+/-22 versus 70+/-12 mU of TF/1000 monocytes, P=0.02). This increase was blunted by L-arg (43+/-16 mU of TF/1000 monocytes, P=0.01). CONCLUSIONS: This study demonstrates that angioplasty-induced plaque rupture is associated with a marked increase in monocyte TF response that is blunted by the oral administration of L-arg. This suggests that the documented antithrombotic properties of NO may be related in part to an inhibitory effect on monocyte TF response.

Angioplasty, Balloon↗
PubMed1998

[Primary biliary cirrhosis associated with pericardial effusion].

The authors report a case of primary biliary cirrhosis, associated with moderate pericardial effusion, in a patient with antiphospholipid antibodies. The pericardial effusion resolved, and did not recur, in response to treatment with Colchicine and ursodesoxycholic acid.

Cholagogues and Choleretics↗
PubMed1997

[Mobile thrombi of the right heart in pulmonary embolism].

Systematic transthoracic echocardiography in all cases of pulmonary embolism may demonstrate right heart thrombi. The results of this monocentric series of 28 consecutive cases observed between 1987 and 1996 were analysed. Twenty-four patients were in NYHA Class IV: thirteen were in cardiogenic shock. Echocardiographic signs of acute cor pulmonale were usually observed: 96.3% of patients had right ventricular dilatation, 85.2% paradoxical interventricular septal motion, 88.9% pulmonary hypertension. The thrombus was typical serpentine (27/28 cases) arising from the lower limb veins. Passage into the left heart chambers through a patent foramen ovale was observed in 3 cases. Pulmonary embolism was confirmed in all cases. This is an extreme therapeutic emergency and 13 patients (46.4%) died despite treatment: surgery (7/16), thrombolysis (2/5), heparin (3/4) or interventional radiology (1/3). After the acute phase, the prognosis was generally good, as demonstrated by the 100% survival rate at 28.6 +/- 25 months. This study confirms the gravity of mobile right heart thrombi in pulmonary embolism. The diagnosis is echocardiographic. No significant difference in mortality was observed between the different therapeutic approaches used in this series. The echocardiographic finding of these thrombi is a traditional indication for emergency surgical embolectomy. Thrombolysis is rapid and readily available and seems to provide promising results alone or before surgery. In patients with contraindications to thrombolysis, interventional radiology or simple heparin therapy may be proposed.

Adult↗
PubMed1996

[Current status of treatment of chronic cardiac insufficiency].

When there is no correctable cause, cardiac failure continues to progress and outcome is poor. However several controlled clinical trials have shown that several therapeutic agents relieve symptoms, improve exercise tolerance and, for some, reduce mortality. Patients in NYHA functional class II, III and IV, whose systolic function is impaired should be treated by digitalis, diuretics and angiotensin-converting-enzyme inhibitors. These therapeutic agents are complementary and each of them are required. Moreover a study has shown that the impairment of patients in NYHA functional class I (who are still asymptomatic but with a ventricular ejection fraction < 35%) could be slowed by angiotensin-converting-enzyme inhibitors. In each case, it is of paramount importance to exclude treatable causes of heart failure because the best the symptomatic treatment can do is slow the inevitable worsening of the disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Acute myocarditis caused by toxoplasmosis simulating infarction. Apropos of a case].

Acute myocarditis due to toxoplasmosis infection has been previously reported, usually in patients suffering from immuno-depression. Cardiac involvement by toxoplasmosis is rare in subjects with a normal immunological status. The authors report the case of a 16-year-old patient without immuno-depression with acute myocarditis caused by toxoplasmosis simulating myocardial infarction.

Acute Disease↗
PubMed1996

[Aortitis in Horton disease. Review of the literature].

First described in 1937, giant cell aortitis (aortitis associated with giant cell arteritis) occurs in 20 to 40% of patients with giant cell arteritis and is often clinically silent. Temporal involvement usually precedes aortic involvement. The process may involve the entire aorta, but complications are usually related to thoracic involvement. Patients with giant cell aortitis may be asymptomatic, or present with aortic arch syndrome, dilation of the aorta, aortic aneurysm, aortic dissection, sudden rupture of the aorta, or aortic valve incompetence. Thoracic aneurysms are usually fusiform and can be complicated by dissection in up to 50% of patients. Aortic involvement may be the presenting feature of giant cell arteritis: it may also occur in patients with preexisting temporal arteritis, often when corticosteroid therapy is reduced or discontinued. Aortic rupture complicating aortitis may be the cause of death in 3-12% of patients with giant cell arteritis. Clinical follow-up with assessment of disease activity by chest X-ray and biological markers of inflammation should be performed yearly in giant cell arteritis. Aortic involvement should be suspected if cardiac or vascular echo-Doppler shows evidence of an aortic arch syndrome, aortic dilation, aneurysm, or of aortic valve incompetence. Corticosteroid therapy, beginning with a dose of 1 mg/kg/day remains the key point of therapy. The dose is subsequently adjusted based on the clinical course and the results of ancillary tests. This treatment might prevent fatal outcome with aortic rupture. Long-term follow-up of all patients with giant cell arteritis or polymyalgia rheumatica is essential, as complications may develop late in the course of the disease.

Aortitis↗
PubMed1995

[Doppler echocardiography in the evaluation of left ventricular diastolic function].

It is now well recognized that a disorder of left ventricular filling can be sufficient to account for congestive heart failure. Furthermore, evaluation of heart disease would not be complete if it did not include assessment of left ventricular filling, improvement of which probably ensures better control of the heart disease. An efficient and reliable tool for the study of diastolic function is therefore essential. The authors review the current state of knowledge and the more recent developments in Doppler echocardiography in the evaluation of left ventricular diastolic function. After revising the pathophysiology, the methods of studying ventricular filling are described. The recording technique is described, taking into account recent developments in transthoracic and transoesophageal approaches. This investigation provides parameters allowing semiquantitative estimation of filling pressures (mean left atrial pressure, end-diastolic pressure) and reliable evaluation of overall diastolic performance.

Adult↗
PubMed1994

Evidence for time-dependent activation of monocytes in the systemic circulation in unstable angina but not in acute myocardial infarction or in stable angina.

BACKGROUND: Platelet activation plays a pivotal role in the pathogenesis of acute coronary disease. Monocytes are involved in the progression of atherosclerosis and are potent activators of blood coagulation through their ability to synthesize tissue factor (TF). The aim of this study was to compare markers of monocyte and coagulation activation in the systemic blood of patients with unstable angina, acute myocardial infarction, or stable angina. METHODS AND RESULTS: We studied 26 patients with unstable angina (10 +/- 5 hours after the onset of the last episode of pain), 18 patients with acute myocardial infarction (5 +/- 4 hours after the onset of pain), and 34 patients with stable angina. We measured levels of TF expression in peripheral blood mononuclear cells (isolated by gradient centrifugation and incubated for 16 hours, with or without endotoxin stimulation), levels of plasma prothrombin fragment 1 + 2 (F1 + 2), and levels of fibrinogen in peripheral blood. In patients with unstable angina, both stimulated and unstimulated cells exhibited higher levels of TF expression than in patients with stable angina (P = .0001). In patients with acute myocardial infarction, monocyte TF activity did not differ from that in patients with stable angina. Mean levels of F1 + 2 and of fibrinogen did not differ significantly between groups. Only in the unstable angina group, a modest correlation was found between fibrinogen (r = .72, P = .005) and F1 + 2 levels (r = .54, P = .001) levels and the degree of monocyte TF expression. In patients with unstable angina, monocyte TF expression (both stimulated and unstimulated, assessed by biological activity and by antigen techniques) and fibrinogen levels were correlated with the time elapsed from the beginning of the most recent episode of pain (.61 < r < .72, .02 < P < .0001). By contrast, there was no correlation between these variables and the time from onset of pain in patients with acute myocardial infarction. CONCLUSIONS: A time-dependent activation of systemic monocytes and a time-dependent increase in fibrinogen levels occurs in unstable angina but not in myocardial infarction. These findings provide further evidence that a specific inflammatory process occurs in unstable angina. Further studies are required to determine whether monocyte activation is a cause or a consequence of plaque instability in patients with unstable angina and to clarify the interrelations between platelet and monocyte activation in these circumstances.

Adult↗
PubMed1994

[Fissuration of thoracic aneurysm in Horton disease, favourable course after surgery].

The authors report another case of rupture of the thoracic aorta in Giant Cell arteritis. The progressive nature of the rupture enabled life-saving aortic replacement with a vascular prosthesis. Only one previous report of this type of operation was found in a search of the literature. The prevalence of aortitis in Giant Cell arteritis would appear to be underestimated after autopsy studies. It affects the thoracic aorta mainly in the ascending segment but sometimes involves the whole aorta. It may remain asymptomatic or be complicated by arterial occlusion, aortic regurgitation, aneurysm, dissection or rupture. Effective steroid therapy could prevent these complications.

Aged↗