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Biomedical subjects

I Sheiban

Publications and source records attributed to I Sheiban.

At least 37 records · Page 2Linked to original sources
PubMed1998

Wiktor stent for treatment of chronic total coronary artery occlusions: short- and long-term clinical and angiographic results from a large multicenter experience.

OBJECTIVES: This study reports the first multicenter experience with the Wiktor coil stent for treatment of chronic total coronary artery occlusions (CTOs). BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) of CTO is associated with very high restenosis and reocclusion rates. Coronary stenting has been proposed as a means of improving outcome. However, the Wiktor device for CTOs has never been tested in a large patient sample. METHODS: From January 1993 to December 1996, 89 patients with 91 CTOs underwent Wiktor stent implantation after successful PTCA. The post-stenting regimen consisted of warfarin (Coumadin) plus aspirin in the initial 49 patients (55%) and aspirin plus ticlopidine in 40 patients (45%). RESULTS: Stenting was successful in 87 patients (98%). At 1 month, 6% of patients had subacute stent thrombosis, 3% had a major bleeding event, and 1% had access-site complications. Subacute stent thrombosis showed univariate association with warfarin therapy (p = 0.009). Angiographic follow-up was obtained in 76 (93%) of 82 eligible patients. The restenosis rate was 32%, including 4% reocclusions. By multiple logistic regression analysis, restenosis was independently associated with multiple stents (adjusted odds ratio [OR] 27.67, 95% confidence interval [CI] 4.25 to 79.95, p = 0.0008) and increasing values of occlusion length (adjusted OR 1.23, 95% CI 1.09 to 1.39, p = 0.001). Freedom from death, myocardial infarction or stented vessel revascularization was 87% and 72% at 1 and 3 years, respectively. CONCLUSIONS: Short- and long-term clinical and angiographic outcomes are favorable in patients undergoing Wiktor stent implantation in CTO. Further technical improvement is needed to reduce the restenosis rate in patients with long lesions and multiple stents.

Analysis of Variance↗
PubMed1997

Recovery of left ventricular function following early reperfusion in acute myocardial infarction: a potential role for the calcium antagonist nisoldipine.

The purpose of the present study was to test whether the administration of a vascular-selective organic calcium antagonist (nisoldipine) at the onset of early mechanical reperfusion (by coronary angioplasty) in acute myocardial infarction could prevent or attenuate postischemic stunning and enhance the recovery of left ventricular function in these patients. The study included 36 patients with anterior acute myocardial infarction who underwent an early and successful primary coronary angioplasty within 3 hours of the onset of chest pain (mean time to reperfusion = 113 +/- 37 minutes). The infarct-related artery was the left anterior descending artery in all patients. All had single-vessel disease. Baseline coronary arteriography was completed by left ventriculography. When the infarct-related artery was identified, a guidewire was placed into the target vessel and a balloon catheter was positioned in the artery. At this point all patients were administered 0.8 mg of intracoronary nitrates through the guiding catheter. Patients were then randomized. Seventeen patients (the NIT group) did not receive further treatment during the procedure, while the other 19 patients (the NIS group) received an additional 0.05 mg of intracoronary nisoldipine. Postprocedure treatment consisted of oral nitrates (80-120 mg/day) plus enalapril (10-20 mg/day) in the NIT group patients, and oral nisoldipine (20 mg/day) plus enalapril (10-20 mg/day) in the NIS group patients. The same treatment was maintained during the 6-month follow-up period. An echocardiographic study was performed at 1, 7, 30, 90, and 180 days following the procedure. Left ventriculography and coronary angiography were repeated at 1 and 180 days after the mechanical reperfusion. An exercise test was performed at 30, 90, and 180 days following primary angioplasty. Left ventriculograms and two-dimensional echocardiograms were analyzed by a computerized system that evaluated left ventricular volumes, ejection fraction, segmental wall motion, and diastolic function (from the left ventricular volume curve). Under baseline conditions, the clinical and angiographic characteristics of the patients were similar in both treatment groups. The results showed a significantly earlier recovery of left ventricular systolic and diastolic function in the NIS group patients compared with those of the NIT group. Also, exercise capacity was significantly better at 30 days in the NIS group. The findings of the present study provide further evidence that early reperfusion in acute myocardial infarction is likely to be followed by myocardial stunning. The vascular-selective organic calcium antagonist nisoldipine, administered at the onset of reperfusion, seems to attenuate postischemic stunning and to enhance the recovery of left ventricular function in this clinical subset.

Acute Disease↗
PubMed1997

[Immediate and long-term clinical and angiographic results of the Wiktor stent in the treatment of chronic coronary occlusions].

BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA) of chronic total coronary artery occlusions is associated with very high restenosis and reocclusion rates. Coronary stenting has been proposed as a means of improving outcome. However, the Wiktor device for chronic coronary occlusion has never been tested in a large patient sample. This study reports the first multicenter experience with the Wiktor stent for treatment of chronic occlusions. METHODS: From January 1993 to December 1996, 89 consecutive patients with 91 chronic occlusions underwent Wiktor stent implantation after successful PTCA. Post-stenting regimen consisted of coumadin plus aspirin in the first 49 (55%) patients and aspirin plus ticlopidine in the following 40 (45%). RESULTS: Stenting was successful in 87 (98%) patients. At 1 month, 6% of patients had subacute stent thrombosis, 1% access-site complications and 3% major bleeding events. Stent thrombosis showed a univariate association with coumadin therapy (p = 0.009). Angiographic follow-up was obtained in 93% of 82 eligible patients. Restenosis rate was 32%, including 4% reocclusions. Through multiple logistic regression analysis, restenosis was independently associated with multiple stents (odds ratio-OR = 27.67, 95% confidence interval-CI = 4.25 to 79.95, p = 0.0008) and increasing values of occlusion length (OR = 1.23, 95% CI = 1.09 to 1.39, p = 0.001). Freedom from death, myocardial infarction or stented vessel revascularization was 87 and 72% at one and three years, respectively. CONCLUSIONS: Short- and long-term clinical and angiographic outcomes are favorable in patients undergoing Wiktor stent implantation for chronic coronary occlusion. Further technical refinements are needed to reduce restenosis rate in patients with long lesions and multiple stents.

Analysis of Variance↗
PubMed1996

Left ventricular diastolic function during adrenergic stress in essential hypertension: acute and chronic effects of ACE inhibition.

We studied the changes in left ventricular (LV) diastolic function induced by angiotensin-converting enzyme (ACE) inhibition at rest and during adrenergic stimulation and their relation to blood pressure (BP) variations to determine whether reductions in the renin-angiotensin system may improve diastolic function irrespective of BP reduction. Echocardiographic indices of systolic and diastolic function, plasma catecholamines as estimated by high-pressure liquid chromatography, and BP variations (Dynamap) were determined at rest and during the cold pressor test (CPT) before and 6 hours and 20 days after ACE inhibition (lisinopril), 20 mg/day by mouth in 10 subjects with uncomplicated essential hypertension. Blood Pressure was significantly reduced after both 6 hours and 20 days of therapy. The cold pressor test induced similar increases in BP in both basal conditions and after acute and chronic treatment. Catecholamine levels were unchanged by the therapy. Systolic function, evaluated by fractional shortening, ejection fraction, and systolic dV/dt, was normal and unchanged during CPT and after treatment. Diastolic function, assessed by volume curve analysis, showed a reduced percentage contribution of rapid filling to total diastolic filling, an increase in the contribution of the atrial systole, and an increase in the isovolumetric relaxation time. During CPT these parameters deteriorated further in response to increased afterload. Lisinopril therapy induced significant increases in end-diastolic volume (p < 0.005) with a progressive increase in the rapid filling dV/dt (p < 0.005 at rest; p < 0.001 during CPT) and a reduction in isovolumetric relaxation (p < 0.0001 at rest and p < 0.01 during CPT). The correlation between systolic BP (afterload) and the rapid filling dV/dt, both at rest and during CPT, was modified by treatment with the ACE inhibitor, with significantly higher rapid filling dV/dt values, and with the pressure loads equal (reduction of the slope and rightward shift of the correlation line). The improvement in diastolic function achieved by ACE inhibition at rest and during CPT appears unrelated to plasma catecholamines and only partly ascribable to the reduced pressure load. The tissue angiotensin II reduction might by itself improve the myocardial response to the pressure load and adrenergic stimulation.

Adult↗
PubMed1996

Correlation between peripheral hemodynamic changes and left ventricular diastolic function in hypertensive patients treated with urapidil.

We evaluated the modifications induced by chronic treatment with an alpha 1-adrenolytic hybrid drug, urapidil, on the hemodynamic parameters in peripheral artery and left ventricle diastolic function. Fifteen mild to moderate essential hypertensive patients (13 men, 2 women; mean age 42 years, range 32-54 years) received urapidil (60 mg b.i.d.) for 6 months. Peripheral hemodynamic and cardiac parameters were evaluated by duplex scanner, coupled with a plethysmographic method, basally (T0) and after 6 weeks' (T1) and 6 months' treatment (T2). Mean blood pressure (BP) showed a reduction after 6 weeks of -9.07 mm Hg (confidence intervals [CI] 95%: -9.21; -8.92; P < 0.01), which was maintained after 6 months (-8.21 mm Hg, CI 95%: -8.97; -7.43; P < 0.01), while no significant change was seen in heart rate. Compliance showed highly significant changes after both 6 weeks (+1.073 dyn-1.cm4.10(-7), 95% CI: +0.965; +1.181, P < 0.001) and 6 months (+0.933 dyn-1.cm4. 10(-7), 95% CI: +0.903; +0.963, P < 0.001), as well as characteristic impedance (T1:-16.689 dyn.s.cm-5/10(2), 95% CI: -16.914; -16.463 P < 0.001; T2: -15.98 dyn.s.cm-5. 10(2), 95% CI: -18.186; -13.784; P < 0.001) and forearm resistances (T1: -26.153 mm Hg.ml-1.s, 95% CI: -34.553; -17.753, P < 0.01; T2: -43.587 mm Hg.ml-1.s, 95% CI: -52.711; -34.464, P < 0.01). Similarly, we have recorded a similar change in left ventricular end-diastolic posterior wall thickness (T1: -1.067 mm, 95% CI: -1.099; -1.035, P < 0.01; T2: -2.866 mm, 95% CI: -3.044; -2.688, P < 0.01), end-diastolic interventricular septum thickness (T1: -0.921 mm, 95% CI: -1.511; -0.289, P < 0.05; T2: -2.711 mm, 95% CI: -3.211; -2.199, P < 0.01), end-diastolic volume (T1: +6.4 ml, 95% CI: +6.343; +6.456, P < 0.01; T2: +19.867 ml, 95% CI: +18.564; +21.170, P < 0.01), and mass/volume index (T1: -0.11, 95% CI: -0.118; -0.101, P < 0.01; T2: -0.218, 95% CI: -0.221; -0.217, P < 0.01). Changes in arterial compliance have shown a statistically significant correlation with changes in mass/volume index (r = -0.468; P < 0.03), end diastolic volume (r = 0.501; P < 0.02), as well as left ventricle rapid filling phase (r = 0.426; P < 0.05) and left ventricle end diastolic posterior wall thickness (r = -0.478, P < 0.03). Our results suggest that the antihypertensive efficacy of urapidil coupled with the restoration of the dumping function of the large arteries, and the reduced activation of reflex sympathetic activation, may play a considerable role among the mechanisms allowing the regression of the functional modifications affecting the left ventricular diastole.

Adult↗
PubMed1995

Clinical and therapeutic implications of chronic left ventricular dysfunction in coronary artery disease.

In patients with myocardial ischemia, left ventricular dysfunction (LV) may arise from irreversible damage (cell death), myocardial stunning (postischemic dysfunction), or myocardial hibernation (persistent myocardial dysfunction at rest due to underperfusion). Chronic LV dysfunction usually refers to hibernating myocardium. However, stunning might also become chronic, producing persistent myocardial dysfunction. Clinical studies have demonstrated that many patients with coronary artery disease have subsequent recurring ischemic (symptomatic or silent) episodes at short intervals in the same area and that each episode may be followed by myocardial stunning. In these patients the myocardium may not recover fully between episodes and function may remain reversibly depressed for long periods or may even be clinically depressed. The recognition of both stunning and hibernation is very important clinically and therapeutically, since chronic LV dysfunction may have a negative effect on mortality and morbidity in patients with coronary artery disease. Moreover, both clinical states are potentially correctable. Pharmacologic intervention with beta blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists might improve or protect hibernating myocardium. The acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine have been investigated in patients with chronic LV dysfunction probably arising from hibernating myocardium. Nisoldipine was found to improve both left ventricular systolic and diastolic function without activating the adrenergic system. The improvement in systolic function may be due to a redistribution of coronary blood flow and to a slight reduction in afterload induced by nisoldipine. On the other hand, nisoldipine may improve diastolic function in these patients by an intrinsic mechanism, Reducing intracellular calcium overload or balancing intracellular calcium homeostasis in the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic Disease↗
PubMed1995

[Myocardial hypertrophy and arterial hypertension].

Myocardial hypertrophy in different cardiac diseases is considered to be an adaptive mechanism to the increase of hemodynamic load which might restore to normal radius/wall thickness ratio and consequently to normalize wall stress. However, it has been widely demonstrated that beside the hemodynamic load, other factors contribute to the development of myocardial hypertrophy. It has been shown that in hypertensive patients, functional abnormalities (increased contribution of atrial systole to total diastolic filling, increased isovolumic relaxation period, prolonged diastolic duration, slowed ventricular filling and altered diastolic distensibility) precede the development of myocardial hypertrophy. Thus, in hypertensive patients, sign and symptoms of heart failure could be manifested in absence of myocardial hypertrophy, and might be exclusively due to diastolic dysfunction (with normal systolic function). Systolic function might be involved and compromised late when focal myocardial cell death and fibrosis occur and consequently ¿adequate¿ hypertrophy is shifted to ¿inadequate¿. This evolution is accompanied by morphological and functional changes of the myocardium similar to those encountered in dilated cardiomyopathy. Impairment of systolic function in ¿inadequate¿ hypertrophy is also due to structural changes; altered ratio between sarcomers and mitochondria, increased intercapillary distance, sarcoplasmatic reticulum dysfunction, increase of collagene component with a consequent increment of wall rigidity, hypertrophy of arterial tunica media, which alters coronary flow and coronary reserve. The progression of these morpho-functional abnormalities is a very slow process, in which adaptive mechanism mediated by several enzymes and contractile protein, contribute to maintain myocardial viability. However, over the long course, disseminated focal myocardial cell necrosis and fibrosis, which is an evolving process, is considered to be the main responsible factor for the irreversible myocardial damage and systolic dysfunction in advanced myocardial inadequate hypertrophy.

Cardiomegaly↗
PubMed1994

[Elements conditioning the severity of myocardial infarction damage].

The severity of myocardial damage following acute myocardial infarction (AMI) is essentially influenced by the duration of coronary flow interruption during the acute episode. Furthermore the duration and severity of "culprit" lesion before AMI, as well as the presence of adequate collaterals to the culprit vessel represent important factors able to influence the severity of myocardial dysfunction after AMI. Left ventricular damage might evolve progressively depending on the infarct size, the presence of diffuse and severe coronary artery disease and concomitant systemic disease, such as diabetes and systemic hypertension. From a therapeutic point of view, in the presence of irreversible myocardial damage (scar tissue) following AMI medical therapy must be addressed to reduce myocardial consumption and to prevent ventricular dilatation. However myocardial dysfunction following AMI might be reversible (hibernated myocardium). It is of remarkable value the recognition of the hibernated but viable tissue because restoration of normal blood flow, which is the gold standard therapy in these patients, improves myocardial function and clinical outcome in AMI patients. In the presence of hibernated tissue following AMI, pharmacological therapy might temporarily protect the hibernated areas; however, when restoration of normal blood flow (myocardial revascularization) is not performed early, myocardial dysfunction might worsen and progressively evolve becoming irreversible event with restoration of normal coronary flow.

Cardiomegaly↗
PubMed1994

[Mechanisms of transluminal mechanical coronary recanalization].

Coronary angioplasty (PTCA) represents one of the most diffuse technique for myocardial revascularization in coronary artery disease patients. The principal mechanisms, responsible for the luminal increment after successful balloon dilatation are stretching of the vessel wall and splitting of the plaque and its rearrangement in an increased cross section of the vessel. Soon after balloon deflation elastic recoil of the vessel wall might occur at different grades which result in a partial loss of the result achieved by balloon PTCA. This phenomenon seems to be one of the major factors influencing the acute and long-term results of PTCA. Balloon inflation is also followed by endothelial denudation and intramural hemorrhage and intramural thrombus apposition. Then, a proliferative process takes place which is characterised by intimal and smooth muscle proliferation and migration. This process, beside the elastic recoil of the vessel wall, might also contribute to restenosis following balloon PTCA. Other devices for myocardial revascularization were introduced in the clinical practice based on different mechanisms from that of conventional PTCA. Transluminal atherectomy (directional, rotational and rotational-ablation) is based on the removal of plaque material from the vessel, increasing the lumen and creating a smooth surface. By this mechanism of action, plaque splitting and vessel wall stretching might be avoided, thus acute and long-term results are supposed to be improved as compared to balloon angioplasty. Another device for the removal of plaque material is represented by laser angioplasty which utilizes laser energy for the evaporation of the atherosclerotic material and the increase of vessel lumen without vessel wall stretching and plaque splitting.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1994

Changes induced by nicardipine slow release in forearm and myocardial hemodynamics of subjects with essential hypertension.

OBJECTIVE: To evaluate the modifications induced by chronic treatment with a new formulation of nicardipine (slow release) on the hemodynamic parameters in peripheral artery and left ventricle diastolic function. MATERIALS AND METHODS: Ten mild to moderate essential hypertensive male patients (mean age 42 years, range 32-54 years) received nicardipine slow release (40 mg b.i.d.) for six months. Peripheral hemodynamic and cardiac parameters were evaluated by duplex scanner, coupled with a plethysmographic method, basally (T0) and after 1 (T1) and 6 months' treatment (T2). RESULTS: Blood pressure showed a significant reduction after 1 month (mean blood pressure 109 +/- 2 vs 124 +/- 3 mmHg, M +/- SE, p < 0.001), which was maintained after 6 months (mean blood pressure 112 +/- 3 mmHg, p < 0.001), while heart rate showed only a slight, non-significant increase. There were highly significant changes in distensibility (0.29 +/- 0.02 vs 0.16 +/- 0.01 s2.cm-2, T2 vs T0, p < 0.001), characteristic impedance (55 +/- 3 vs 78 +/- 3 dyn.s.cm-5.10(2), T2 vs T0, p < 0.001) and local resistances (71 +/- 5 vs 118 +/- 4 mmHg.ml-1. s, T2 vs T0, p < 0.001) in the brachial artery, and also in left ventricle posterior wall diastolic thickness (10.2 +/- 0.4 vs 11.5 +/- 0.3 mm, T2 vs T0, p < 0.05), end diastolic volume (127 +/- 3 vs 109 +/- 3 ml, T2 vs T0, p < 0.01) and mass/volume index (1.21 +/- 0.03 vs 1.35 +/- 0.03, p < 0.05). CONCLUSIONS: The antihypertensive efficacy of nicardipine slow release, with only two daily administrations, allows the restoration of the dumping function of the large arteries, and the regression of the functional modifications affecting the left ventricular diastole.

Adult↗
PubMed1993

Interrelation between angiographic severity of coronary artery disease and plasma levels of insulin, C-peptide and plasminogen activator inhibitor-1.

Plasma insulin, C-peptide and plasminogen activator inhibitor-1 (PAI-1) levels were measured in 64 men with coronary artery disease (CAD) documented by angiography. Coronary arteriograms were analyzed, and the severity and diffusion of coronary lesions were quantified by score systems. C-peptide and PAI-1 levels in patients with CAD were significantly higher than in 30 control subjects. Insulin, C-peptide and PAI-1 showed a highly significant correlation with the severity scores for coronary lesions (C-peptide more than insulin), but only a weak correlation with diffusion scores. Highly significant correlations were found between insulin and PAI-1, and even greater ones between C-peptide and PAI-1. It has been proposed that hyperinsulinemia may be involved in the etiology of atherosclerotic cardiovascular disease by dysregulating lipoprotein metabolism and blood pressure. These findings support that hypothesis and suggest that insulin secretion may be an index of the severity of CAD. Because a direct effect of insulin on the cells that synthesize PAI-1 has been shown, the present data further indicate that the effect of insulin on fibrinolysis may be another way by which hyperinsulinemia accelerates atherogenesis.

Body Mass Index↗
PubMed1993

Left ventricular dysfunction following transient ischaemia induced by transluminal coronary angioplasty. Beneficial effects of calcium antagonists against post-ischaemic myocardial stunning.

Acute and severe ischaemia is followed by depression of myocardial contractility during reperfusion; return to full recovery might take a long time. This phenomenon, termed myocardial stunning, has been extensively demonstrated in experimental studies and in different clinical settings. The beneficial effects of calcium antagonists in preventing post-ischaemic myocardial stunning have been tested in experimental studies, showing that when administered before or during ischaemia, they inhibit post-ischaemic myocardial dysfunction. The present study was undertaken to verify the possible occurrence of myocardial stunning following transient ischaemia induced by coronary angioplasty. The aim was also to evaluate the possible protective effects of calcium antagonists (nisoldipine) and nitrates against myocardial stunning in patients with coronary artery disease undergoing routine coronary angioplasty (PCTA) with prolonged inflation. The study included 25 patients, aged between 40 and 69 years, with exercise-induced angina and single vessel disease. The stenosis was severe (80% to subtotal occlusion), localized on the left anterior descending artery, but without collaterals at coronary angiogram. All patients had normal left ventricular (LV) overall function and normal systolic thickening of the anterior wall supplied by the diseased artery. Our data suggest that post-ischaemic myocardial stunning is not only an experimental curiosity, but that it does occur in different clinical settings. Calcium antagonists (i.e. nisoldipine), when added before or during ischaemia, seem to prevent myocardial stunning. These findings confer a potential role to these agents in the treatment of post-ischaemic myocardial dysfunction.

Adult↗
PubMed1993

[Role of direct coronary angioplasty in the course of acute myocardial infarction].

The application of coronary angioplasty (PTCA) for early mechanical reperfusion in patients with evolving acute myocardial infarction (AMI) was introduced at the beginning of the '80s. There are 5 distinct approaches to PTCA for AMI mainly based on the timing of the intervention: primary or direct PTCA refers to emergency recanalization (as soon as possible) of the "culprit" vessel by the interventional procedure without the use of thrombolytic agents; immediate or sequential PTCA is the combination of administration of intravenous thrombolytic therapy followed very closely by PTCA; rescue PTCA refers to the use of PTCA as a mechanical approach for reperfusion when thrombolytic therapy has failed (60 to 120 min after such therapy has been initiated); deferred or adjunctive PTCA implies coronary angiography and PTCA delayed by at least several days after thrombolytic therapy and reserved for patients with residual ischemia; elective PTCA refers to a delayed symptom-derived procedure after thrombolytic therapy. Immediate PTCA, in which the procedure urgently follows the thrombolytic therapy has been studied in 3 randomized trials (TAMI 1, ECoS, TIMI 2A). All 3 trials have shown that immediate PTCA does not affect positively, but can worsen, the outcome of thrombolytic therapy since it increases mortality and bleeding complication with no improvement in reocclusion rate. Rescue PTCA was evaluated by several Authors who were able to demonstrate that mechanical reperfusion after failed thrombolytic therapy improves prognosis and reduces in-hospital and long-term mortality in this subgroup of patients with AMI. Deferred or adjunctive and elective PTCA represent therapeutic approaches in patients with residual ischemia following a successful thrombolysis able, when residual or recurrent ischemia are present, to prevent major cardiac events and to improve clinical outcome. The major interest was addressed to the role of primary PTCA in evolving AMI, as alternative therapy to thrombolysis. Randomized trials have been able to demonstrate that primary PTCA could dramatically improve the clinical outcome in AMI complicated by cardiogenic shock. Moreover, this approach can be safely performed in patients with contraindications for thrombolytic therapy with excellent results. Despite other advantages, primary or direct PTCA for evolving AMI is still presenting few points which have to be furtherly evaluated: acute or subacute reocclusion rates, restenosis rates, costs and availability to majority of population. The on-going clinical evaluation of other devices for mechanical reperfusion (transluminal extraction catheter-TEC, directional atherectomy, coronary stents, thermal PTCA, prolonged autoperfusion), in order to improve acute and subacute results, could furtherly expand the use of this approach in AMI-patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

[Coronary angioplasty. Indications, diagnostic and indicative methods, follow-up results].

Coronary angioplasty (PTCA) represents a valid alternative to coronary artery bypass surgery (CABG) in several cases; moreover, PTCA might be performed, for myocardial revascularization, even in patients in whom CABG is transitory or definitely contraindicated. However, the guidelines for mechanical myocardial revascularization are still mainly based on clinical criteria and the only angiographic data should not be sufficient to extend the indications for PTCA. Despite the technical improvement of the procedure and the material used, PTCA continues to have two main limitations: the relatively high acute complications rate (4-7%) and long-term restenosis rate (20-40%). The advent of new techniques for myocardial revascularizations (transluminal atherectomy, coronary stents, laser angioplasty) might partially reduce these limitations.

Angioplasty, Balloon, Coronary↗
PubMed1992

Relation of body fat distribution in men and degree of coronary narrowings in coronary artery disease.

This study evaluates the relation between body fat distribution and severity of coronary artery disease (CAD). The study sample comprised 33 patients with angiographically demonstrated CAD and 10 angiographically normal control subjects. Body fat distribution was estimated by computed tomography and degree of coronary narrowings by angiographic score. Body weight, body mass index and total and subcutaneous abdominal adipose tissue areas showed no statistical differences in the 2 groups; visceral abdominal adipose tissue area and the visceral to subcutaneous abdominal adipose tissue area ratio were significantly higher in patients with CAD (p < 0.05). There was a significant correlation between visceral fat and triglycerides, apoprotein B and sum of glucose and insulin during glucose oral tolerance test. Sum of insulin during glucose oral tolerance test, visceral abdominal adipose tissue area and visceral/subcutaneous abdominal adipose tissue area ratio correlated significantly with severity of CAD, as evaluated by coronary score in all subjects and in CAD patients alone. Stepwise multiple regression analysis using the coronary score as the dependent variable and anthropometric and metabolic parameters as independent variables shows that in all subjects and in CAD patients alone, visceral/subcutaneous abdominal adipose-tissue area ratio entered the regression first and the sum of insulin during glucose oral tolerance test second. The results suggest that visceral abdominal adipose tissue area and visceral to subcutaneous abdominal adipose tissue area ratio may be cardiovascular risk factors.

Abdomen↗