Biomedical subjects

M Kyriakidis

Publications and source records attributed to M Kyriakidis.

At least 37 records · Page 2Linked to original sources

PubMed1998

Moxonidine effect on microalbuminuria, thrombomodulin, and plasminogen activator inhibitor-1 levels in patients with essential hypertension.

Increased sympathetic activity seems to play an important role in the pathogenesis and development of complications of atherosclerotic origin in patients with essential hypertension (EH). The aim of this study was to evaluate the effect of a new antihypertensive agent, moxonidine (M), on microalbuminuria (urine albumin excretion, UAE), plasma thrombomodulin (TM), and tissue plasminogen activator inhibitor (PAI-1) in patients with mild to moderate EH associated with increased UAE. Fifty-eight patients (32 M, 26 F) with EH and microalbuminuria, with a mean age of 56.6 +/- 8.2 years and a body mass index (BMI) of 23.8 +/- 3.1 kg/m2 who responded to M therapy (0.3-0.4 mg/daily) were studied before and after their blood pressure control. The 24-hour urine albumin excretion (RIA method), as well as TM and PAI-1 plasma levels (ELISA method), were determined before and 6 months after the initiation of treatment under moxonidine therapy. At the end of the 6-month period, all patients remained normotensive. The 24-hour urine albumin excretion had decreased to 24.5 +/- 6.4 vs. 32.3 +/- 7.2 ug/min before therapy (P < 0.001). The plasma TM levels had decreased to 44.0 +/- 7 vs. 51.0 +/- 9 ng/mL before therapy (P < 0.01), and PAI-1 levels had also decreased to 11.5 +/- 4.5 vs. 15.8 +/- 8 IU/mL before therapy (P < 0.05). The results of our study suggest that in hypertensive patients with microalbuminuria, moxonidine, an imidazoline I1-receptor agonist, a new centrally acting antihypertensive agent, significantly reduces urine albumin excretion as well as thrombomodulin and PAI-1 levels. These preliminary findings demonstrate a favorable effect on renal function and endothelial homeostatic mechanisms (maintenance of haemostatic balance).

Albuminuria↗

PubMed1998

Role of transesophageal echocardiography in the diagnosis of infected retained pacing lead.

A 68-year-old woman had a transvenous pacemaker implanted 6 years ago. One year after the procedure the pulse generator was removed due to generator site infection. Efforts to remove the lead resulted in fracture of the tip, which was abandoned in the right cardiac cavities. After this the patient suffered intermittent episodes of fever and chills, which responded to antibiotic therapy. At her recent admission, transesophageal echocardiography revealed a large mass attached to the free end of the fractured lead suggestive of the existence of a vegetation on the pacing lead. The diagnosis was confirmed at surgery.

Aged↗

PubMed1998

Thallium-201 for detection of myocardial viability: comparison of early postexercise reinjection and imaging with 4 and 18-24 hours redistribution imaging.

To evaluate the efficacy of an early 201Tl reinjection and imaging protocol for reducing the need for conventional 4-hour or optimal 24-hour redistribution imaging (RI) and detecting of myocardial viability, we compared the results of early postexercise Tl reinjection and imaging with those of 4- and 24-hour RI in 74 consecutive patients aged 55 +/- 9 years (mean +/- SD) who were assessed for myocardial ischemia. One millicurie of Tl was injected promptly after completion of the initial postexercise imaging (PEX) and three additional sets of images were acquired 1, 4 and 18-24 h later. A total of 2,368 segments were evaluated. On PEX, 390 (17%) segments showed defects, of which 287 (74%) showed enhanced Tl uptake at 1-hour RI; 89 (23%) did not change and 14 (4%) showed reverse redistribution. Of the 103 persistent defects, only 27 (7%) showed further fill-in of Tl; 62 (16%) segments showed reverse redistribution at 4-hour RI while at 18- to 24-hour RI 17 (4%) and 47 (12%) segments showed further fill-in of Tl and reverse redistribution, respectively. Finally, after analysis of 4- and 18- to 24-hour RI, the diagnosis changed from myocardial necrosis to ischemia in only 2 (3%) patients. In conclusion, these results suggest that by eliminating the need for an additional delayed set of images for detection of myocardial viability, this protocol reduces the total investigation procedure, is more convenient for the patient, increases patient turnover and expedites the decision-making process.

Decision Making↗

PubMed1998

Hypertrophic cardiomyopathy in Greece: clinical course and outcome.

OBJECTIVE: Evaluation of clinical course and outcome of hypertrophic cardiomyopathy in a representative Greek population. BACKGROUND: Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy and varied clinical expression. Recent studies suggest ethnic differences. MATERIALS AND METHODS: One hundred seventy-four consecutive Greek patients (117 male, 57 female, age 47+/-16 years) from 143 different families were assessed at the Department of Cardiology of the University of Athens, Greece, and the State Cardiac Department, Hippokration Hospital, both located in Athens, Greece. To reduce selection bias, referral was based on disease diagnosis irrespective of clinical status or treatment needs. All patients were examined clinically, echocardiographically, and by ECG ambulatory monitoring at 6-month intervals for a period of 74+/-22 months (range, 8 to 108 months). RESULTS: Most patients (n = 156, 89.7%) were in New York Heart Association (NYHA) functional class I or II. The disease was familial (at least one affected first-degree relative) in 81 of the 143 families (56.6%), and in 19 of these (13.3%) there was familial history of sudden cardiac death. At initial examination, intraventricular septal thickness was 17.3+/-4.1 mm and posterior wall thickness was 13.7+/-3.8 mm and a left ventricular outflow gradient >30 mm Hg was present in 58 patients (33.3%). Similar were the findings during the last examination (17.5+/-4.3 mm, 13.5+/-4.4 mm, and 56 (32.2%, respectively, p = not significant). Episodes of nonsustained ventricular tachycardia were noted in 15 patients (8.6%). There were eight deaths during follow-up: four sudden deaths and four from intractable heart failure. Syncope was reported by all patients who died. The annual mortality in this study was 1%. Syncope and NYHA class were the only predictors of outcome. CONCLUSIONS: In this representative Greek patient cohort with hypertrophic cardiomyopathy, the arrhythmogenic substrate was modest and the clinical course benign. Sudden cardiac death was infrequent and syncope, functional class, and ventricular arrhythmias were the only predictors of a poor outcome.

Adolescent↗

PubMed1996

Captopril adjuvant therapy to beta-blockers and nitrates improves post-myocardial infarction left ventricular performance.

A growing body of data support the beneficial effects of angiotensin-converting enzyme inhibitors in the prevention of cardiac enlargement and improvement of left ventricular function in patients with acute myocardial infarction. However, very little information exists about the direct effect of increased afterload on cardiac performance in these patients and the possible favourable effects of angiotensin-converting enzyme inhibitors as adjunctive treatment to thrombolysis, beta-blockers and nitrates. We have, therefore, studied the effects of captopril as adjuvant therapy to thrombolysis, beta-blockers and nitrates (standard therapy) on left ventricular performance in 77 consecutive patients with uncomplicated Q-wave acute myocardial infarction, by the measurement of the pre-ejection period/left ventricular ejection time ratio before and after (0.25-0.50 mg) phenylephrine administration on the 4th and 30th post-infarction days. Patients were randomized on day 4 either to continue standard therapy alone (group 1, 35 patients) or to receive oral captopril therapy (12.5 mg t.i.d.) in addition to standard therapy (group 2, 42 patients) in a double-blind parallel study. Among the patients of group 1 there was a significant deterioration of left ventricular function after phenylephrine administration. This was shown by an increase of pre-ejection period/left ventricular ejection time ratio only in the subset of patients with ejection fraction < 40%, as measured by contrast ventriculography, on both the 4th and 30th post-infarction days changing from 0.435 +/- 0.070 to 0.528 +/- 0.101, P < 0.01 and from 0.404 +/- 0.098 to 0.515 +/- 0.092, P < 0.02, respectively. In contrast there were no significant changes in patients with ejection fraction > or = 40%. Among patients of group 2, phenylephrine administration induced a significant increase, only on the 4th day, in pre-ejection period/left ventricular ejection time ratio only in the subset of patients with ejection fraction < 40% changing from 0.410 +/- 0.107 to 0.535 +/- 0.102, P < 0.01. In the remaining patients with ejection fraction > or = 40% there were no significant changes on either the 4th or 30th post-infarction days. Furthermore, a significant improvement was observed after phenylephrine administration in the pre-ejection period/left ventricular ejection time ratio between the 4th and 30th post-infarction days, which changed from 0.535 +/- 0.102 on day 4 to 0.368 +/- 0.052 on day 30 (P < 0.004). Also, a four-way ANOVA detected a significant reduction of heart rate in patients with ejection fraction < 40% from day 4 to day 30. The results indicate that: (1) the response of pre-ejection period/left ventricular ejection time ratio after increasing afterload may be a useful non-invasive method for the detection of left ventricular dysfunction in myocardial infarction patients; and (2) captopril adjuvant therapy as compared to thrombolysis, beta-blockers and nitrates alone, after phenylephrine administration, improves the left ventricular performance response in asymptomatic Q-wave post-infarction patients and beneficially affects heart rate. This effect is most pronounced in patients with ejection fraction < 40% whereas those with ejection fraction > or = 40% do not obtain clear benefit.

Adrenergic beta-Antagonists↗

PubMed1995

An unusually hard lesion in an aortocoronary saphenous vein graft refractory to standard balloon angioplasty.

We report a case of a hard lesion in the body of an aortocoronary saphenous vein graft, which developed 3 years after bypass surgery and was not amenable to dilation during percutaneous coronary angioplasty, despite multiple balloon inflations at pressures reaching 13 atm. Hard lesions in aortocoronary saphenous vein grafts are rare but may lead to balloon angioplasty failure necessitating alternative angioplasty options.

Angioplasty, Balloon↗

PubMed1995

Effect of atrial fibrillation on exercise capacity in mitral stenosis.

To determine the preoperative and postoperative effect of atrial fibrillation (AF) on exercise capacity in mitral stenosis, 12 digitalized patients in AF (7 women and 5 men, age 52 +/- 6.1 years) and 10 in sinus rhythm (5 women and 5 men, age 46 +/- 5 years) underwent maximal cardiopulmonary exercise testing according to Weber's protocol and Doppler echocardiographic examination before and at 3 and 6 months after mitral valve replacement. The ratio of right ventricular acceleration to ejection time was used as an estimate of mean pulmonary artery pressure. Preoperative exercise duration (6.8 +/- 1 vs 8 +/- 2 minutes), peak oxygen consumption (9.7 +/- 3 vs 12.3 +/- 3 ml/kg/min), and right ventricular acceleration to ejection time ratio (0.34 +/- 0.07 vs 0.34 +/- 0.08) were not significantly different between patients with AF and those in sinus rhythm. Postoperative improvement in these parameters was lower in patients with AF than in those in sinus rhythm: exercise duration at 3 months, 7.5 +/- 2 vs 11.9 +/- 2 minutes (p < 0.001); at 6 months, 9 +/- 2 vs 12 +/- 2 minutes (p < 0.001); peak oxygen consumption at 3 months, 10.8 +/- 3 vs 17.5 +/- 3 ml/kg/min (p < 0.001); and at 6 months, 11.9 +/- 3 vs 17.8 +/- 3 ml/kg/min (p < 0.001); right ventricular acceleration to ejection time ratio at 3 months, 0.35 +/- 0.08 vs 0.42 +/- 0.05 (p < 0.05); and at 6 months, 0.38 +/- 0.05 vs 0.44 +/- 0.05 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗

PubMed1995

Sex differences in the anatomy of coronary artery disease.

In a prospective study, the extent and severity of coronary artery disease (CAD) as well as the location of coronary stenoses were studied comparatively, in relation to age and sex, in 192 consecutive women vs 543 selected men, who all underwent coronary angiography during the same time period, and who were found to have significant CAD. Overall, the age of women (59 +/- 8 years) was higher than that of men (55 +/- 8 years), p < 0.001. Also, the prevalence of smoking was higher in men (81% vs 31%, p = 0.0000) and that of diabetes mellitus in women (29% vs 12%, p = 4 x 10(-6)). In addition, women over 50 years old had a higher incidence of hypertension (51% vs 32%, p = 6 x 10(-5)). Although in both sexes the prevalence of multivessel CAD increased with age, the prevalence of one-vessel CAD was significantly more and that of three-vessel CAD significantly less common in women than in men, both overall (35% vs 16%, p = 4 x 10(-8) and 36% vs 54%, p = 2 x 10(-5), respectively) and in all age subgroups. However, the location of coronary stenoses did not show important differences between men and women with the left anterior descending being the most frequently involved artery. Furthermore, the calculated Gensini index, which reflects cumulatively the extent, severity and location of coronary stenoses, was significantly higher in men (59.2 +/- 34.6 vs 52.2 +/- 36.2, p = 0.03), implying more severe and extensive CAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1995

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries.

We studied 12 patients (eight females and four males), ages 30-46 years, with echocardiographically documented mitral valve prolapse and clinical suspicion of coronary artery disease, based on a history of chest pain (five patients), angina-like pain (three patients), a positive exercise stress electrocardiogram (12 patients) and a focally positive thallium-201 stress perfusion scan (three patients), who were referred for cardiac catheterization and found to have normal coronary arteries. Ten patients without evidence of heart disease served as controls. In all mitral valve prolapse patients, coronary flow velocity reserve was determined successively in the left anterior descending, left circumflex and right coronary arteries as the ratio of the maximum (after intracoronary papaverine) to the resting mean coronary flow velocity. Coronary flow reserve values were fairly similar in the mitral valve prolapse and control patients; all 12 mitral valve prolapse patients had normal coronary flow reserve ( > or = 3.5) in all three coronary arteries with no significant differences among the arteries tested. Mean values +/- 1 standard deviation of the coronary flow reserve (mitral valve prolapse vs control patients) were 4.7 +/- 0.5 vs 4.6 +/- 0.6 for the left anterior descending, 4.6 +/- 0.4 vs 4.6 +/- 0.3 for the left circumflex and 4.5 +/- 0.4 vs 4.4 +/- 0.5 for the right coronary artery (all P = non-significant). The subsets of mitral valve prolapse patients with different clinical "ischaemic' manifestations were similar in terms of the calculated coronary flow reserve in all three major epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regional coronary flow reserve does not account for the clinical manifestations of myocardial ischaemia and positive exercise tests in patients with mitral valve prolapse and normal coronary arteries.

Adult↗

PubMed1995

Lack of a thrombotic tendency in patients with acute myocardial infarction and angiographically normal coronary arteries.

The hematological profile of 12 patients with acute myocardial infarction and normal coronary arteriographic findings was compared to that of 8 patients with acute myocardial infarction associated with obstructive coronary artery disease, and of 12 patients with no evidence of myocardial infarction and normal coronary arteriographic and left ventriculographic findings who served as control. There were no significant differences in the hematological profile among the 3 groups, suggesting lack of a thrombotic tendency in patients with acute myocardial infarction and normal coronary arteriographic findings.

Acute Disease↗

PubMed1994

Systolic time intervals after phenylephrine administration for early stratification of patients after acute myocardial infarction.

This study was designed to assess the usefulness of the changes in left ventricular (LV) systolic time intervals after phenylephrine administration for detecting high-risk patients soon after acute myocardial infarction by correlation with the angiographic and ventriculographic findings. The procedure was performed in 76 consecutive patients (group I) on the fourth postinfarction day and in 12 normal subjects (group II) free of coronary artery disease. In 20 patients with LV ejection fraction < or = 40% (subgroup IA) the preejection period (PEP)/LV ejection time (ET) ratio increased from 0.410 +/- 0.107 to 0.535 +/- 0.102 (p = 0.01) after phenylephrine, whereas in the remaining 56 patients (subgroup IB) with LV ejection fraction > 40% and in the 12 normal subjects the PEP/LVET increased nonsignificantly. Of patients with LV ejection fraction > 40% a subset of 20 patients was distinguished with proximal stenosis in both left anterior descending and either a dominant right or left circumflex coronary artery (subset IB-a). In these the PEP/LVET increased from 0.347 +/- 0.056 to 0.445 +/- 0.019 (p = 0.0001) after phenylephrine, whereas in the remaining 36 patients (subset IB-b) without proximal lesions in 2 main arteries the PEP/LVET increased nonsignificantly. In conclusion, the PEP/LVET response to phenylephrine administration early after acute myocardial infarction is a precise, safe, noninvasive bedside method for early stratification of these patients.

Adult↗

PubMed1994

Relation of left atrial volume and systolic function to the hormonal response in idiopathic dilated cardiomyopathy.

We studied the relation of left atrial mechanical function to the hormonal response in 14 patients with idiopathic dilated cardiomyopathy. Left atrial volumes were echocardiographically measured at mitral valve opening (maximal), at onset of atrial systole (onset of the P wave of the electrocardiogram) and at mitral valve closure (minimal) from the apical 2- and 4-chamber views using the biplane area-length method. Left atrial systolic function was assessed with the left atrial active emptying fraction ([volume at onset of atrial systole-minimal]/[volume at onset of atrial systole]). Plasma renin activity, aldosterone and atrial natriuretic peptide plasma levels were determined using commercially available kits. Left atrial maximal volume was directly, and left atrial active emptying fraction was inversely related to plasma renin activity (r = 0.60, P = 0.02 and r = -0.59, P = 0.026, respectively), aldosterone (r = 0.61, P = 0.02 and r = -0.53, P = 0.048) and atrial natriuretic factor (r = 0.79, P = 0.0009 and r = -0.62, P = 0.01) plasma levels. Thus, increased left atrial size and depressed left atrial contractile performance are associated with increased hormonal response in idiopathic dilated cardiomyopathy.

Adult↗

PubMed1994

Factors affecting the postoperative exercise capacity of patients with mitral stenosis and aortic regurgitation.

Factors affecting the exercise capacity of patients with mitral stenosis (MS) and aortic regurgitation (AR) are incompletely understood. Accordingly, exercise capacity was assessed in 13 patients with MS and in 13 with AR by means of cardiopulmonary exercise testing before as well as 3, 6 and 12 months after valve replacement. Left- and right-ventricular function were evaluated echocardiographically. Both in MS and in AR exercise capacity expressed by maximal oxygen consumption (VO2max) increased significantly after valve replacement and was directly related to right ventricular (RV) function assessed by the ratio of RV acceleration time to RV ejection time (r = 0.87, p < 0.001 and r = 0.74, p < 0.001, respectively) and inversely related to left atrial diameter (r = -0.72, p < 0.001 and r = -0.76, p < 0.001, respectively). No relation between VO2max and resting left-ventricular function was found. Thus, the postoperative improvement in the exercise capacity both in mitral stenosis and in aortic regurgitation is associated with an improvement in right-ventricular function and a decrease in left-atrial size.

Aortic Valve Insufficiency↗

PubMed1993

Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings.

To define coronary angiographic characteristics of patients experiencing early primary ventricular fibrillation (VF) in the acute phase of myocardial infarction we studied 266 consecutive patients without clinical evidence of heart failure. Twenty-six patients (group 1) experienced early (< 12 h from the onset of symptoms of myocardial infarction) primary VF whereas 240 patients (group 2) with the same clinical characteristics served as an appropriately matched cohort. All patients were catheterized before or soon after hospital discharge (1 to 8 weeks after the acute event). There was no significant difference in left ventricular ejection fraction between the two groups of patients (39.6 +/- 6% vs 36.9 +/- 8%, P = ns). Patients with early VF had a significantly greater number of diseased vessels than those without VF (3.38 +/- 1.05 vs 2.03 +/- 1.25, P < 0.001) and a higher coronary arteriographic Gensini score (29.31 +/- 4.80 vs 20.16 +/- 4.14, P < 0.001). The left anterior descending coronary artery was identified as the infarct-related vessel in 53.6% of group 1 vs 44.5% of group 2 patients (P < 0.05). The mean maximal serum creatine kinase values were not significantly different (1897 +/- 1062 vs 1426 +/- 839 IU.l-1, P = ns) between the two groups. These data indicate that patients with early primary VF in the setting of acute myocardial infarction may have more extensive coronary artery disease than similar patients without VF. A worse prognosis could be anticipated for these patients on the basis of worse coronary anatomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Plasma atrial natriuretic factor in uncomplicated acute myocardial infarction.

Plasma atrial natriuretic factor (ANF) levels were measured in 29 patients who had normal atrial hemodynamics on days 4 and 8 after an uncomplicated acute myocardial infarction (AMI). All patients had increased ANF levels on day 4. On day 8 of the ANF levels had declined significantly to normal values in 14 patients with enzymatically smaller AMI and higher ejection fractions (> or = 40%), while they remained elevated in 16 patients with larger AMI and lower ejection fractions (< 40%). The study data are compatible with increased secretion of ANF by the more extensively damaged left ventricles in AMI.

Adult↗

PubMed1993

Angina and coronary artery disease in patients with aortic valve disease.

The significance of angina pectoris in patients with aortic valve disease (AVD) and the need for coronary arteriography before valve replacement are controversial. The history of chest pain and coronary arteriographic findings were reviewed in 333 patients > or = forty years old, with AVD: 142 with aortic stenosis, 87 with mixed AVD and 104 with aortic regurgitation. The prevalence of coronary artery disease (CAD) was similar among different types of AVD. Angina pectoris was more frequent in patients with aortic stenosis (56%) and mixed AVD (53%) than in patients with aortic regurgitation (24%) (p < 0.0001). Similar results were found in patients with and without CAD. Twenty-six of 95 (27%) patients with CAD had no chest pain at all. The absence of any chest pain in CAD patients was more frequent in those > or = sixty years old than in those < sixty (p < 0.05). Thus, since a significant number of patients had CAD in the absence of any chest pain, the authors recommend coronary arteriography for all patients > or = forty years of age before aortic valve replacement.

Aged↗

PubMed1992

Correlation of reciprocal ST-segment depression after acute myocardial infarction with coronary angiographic findings.

We studied 266 consecutive patients with acute myocardial infarction to assess the significance of electrocardiographic "mirror images". Ninety-four (group A) had anterior wall and 132 (group B) had inferior wall infarction. Thirty-one group A patients had stenosis of the right coronary artery greater than 85% in diameter (subgroup A1), and 63 either had a normal right coronary artery or less than 85% stenosis (subgroup A2). Of group B patients 62 had greater than 85% stenosis of the left anterior descending (subgroup B1) and 70 had a left anterior descending or less than 85% stenosis (subgroup B2). ST-segment depression was significantly greater in depth and duration in subgroup A1 than A2 (p = 0.02) and in subgroup B1 than B2 (p = 0.02, p = 0.01, respectively). Left ventricular ejection fraction was lower in subgroup A1 than A2 (p less than 0.001) and in B1 than B2 (p less than 0.001). There was a strongly positive correlation between depth and duration of ST-segment depression and the Gensini index (r = 0.78, 0.84) for anterior and inferior infarction, respectively. In conclusion, increased depth and duration of ST-segment depression opposite the infarct are indicative of ischemia, and are related to the extent of coronary artery disease, the degree of stenosis of the vessels supplying the opposite wall and of left ventricular dysfunction.

Aged↗

PubMed1992

Endarteritis of the aortic arch in Turner's syndrome with cystic degeneration of the aorta.

We present a case of a 36-year-old 45 XO Turner syndrome with bicuspid aortic valve, dilatation of the ascending aorta and of the major branches of the aortic arch and multiple cysts of the aortic wall. This was complicated by endarteritis of the base of the aortic arch and production of an intraluminal structure (intra-aortic debris). She also presented reactive pleural effusion and involvement of the pulmonary artery which was complicated by pulmonary embolism. Possible aetiological mechanisms are discussed.

Adult↗