Biomedical subjects

M Kyriakidis

Publications and source records attributed to M Kyriakidis.

47 records · Page 3Linked to original sources

PubMed1992

Early atrial arrhythmias in acute myocardial infarction. Role of the sinus node artery.

We studied atrial arrhythmias during the first 12 h of admission to the hospital in 266 consecutive patients with acute myocardial infarction who subsequently underwent coronary angiography. Ten patients developed atrial fibrillation, one atrial flutter, and one supraventricular tachycardia. Another five developed sinus dysrhythmias. All of the above patients had an acute inferior myocardial infarction, and in 10 of the 12 patients with supraventricular arrhythmias and in four of five with sinus dysrhythmias, the origin of the sinus node artery started just after an occluded right coronary or left circumflex artery or was involved in the occlusion. Thus, ischemia of the sinus node due to coronary occlusion proximal to the origin of the sinus node artery was a likely cause of these arrhythmias.

Adult↗

PubMed1990

Diffusing capacity of the lung and nifedipine in systemic sclerosis.

Lung involvement in systemic sclerosis may be due in part to a functional abnormality of the pulmonary vasculature. To investigate the possible role of a pulmonary vasospastic process in this disorder, 21 non-smoking patients who had no evidence of cardiac disease or pulmonary hypertension were evaluated with pulmonary function tests prior to administration of nifedipine, 30 minutes after a single oral dose of nifedipine (20 mg), and after 4 weeks of treatment with nifedipine (10 mg 3 times daily). Treatment with nifedipine did not significantly change any of the pulmonary function values, except for the carbon monoxide diffusing capacity (DLCO). The linear trend between the individual DLCO values at baseline and their changes immediately following the initial 20-mg dose of nifedipine (r = -0.603, P = 0.02) and after 4 weeks of treatment (r = -0.636, P = 0.01) showed that the lower the DLCO value at baseline, the greater the improvement caused by nifedipine. These findings support the hypothesis of a potentially reversible pulmonary vasospasm in systemic sclerosis and suggest that nifedipine may be useful in the treatment of lung disease in these patients; however, further studies are needed.

Adult↗

PubMed1990

A prospective angiographic study of the coronary collateral circulation in coronary arterial disease.

A prospective angiographic study of the coronary collateral circulation was performed in 600 consecutive patients found to have significant coronary arterial disease at cardiac catheterization. As the number of diseased coronary vessels increased the evidence of collaterals rose significantly (P = 0.00002) and the intensity of the collateral circulation increased (P = 0.05). For totally occluded lesions the collateral incidence was 70.4%, independent of the particular vessel involved. For stenoses greater than 90% collateral frequency and intensity were significantly greater for lesions of the right coronary artery than of the left anterior descending and the left circumflex arteries. The distribution of the coronary collateral circulation is described quantitatively according to the site of the lesion. Finally, a coronary collateral circulation occurred more frequently (P less than 0.000 001) and excepting Grade I, the intensity of the coronary collateral circulation was significantly greater in patients with a history of acute myocardial infarction.

Analysis of Variance↗

PubMed1989

Comparison of haemodynamic effects of nifedipine and molsidomine in patients with coronary artery disease.

The haemodynamic effects of oral nifedipine 20 mg and molsidomine 4 mg were compared in 24 patients with coronary artery disease. Molsidomine unlike nifedipine caused a significant fall in mean pulmonary artery pressure and left ventricular end-diastolic pressure. Both drugs caused a significant and comparable reduction in systolic and diastolic blood pressure. Although only nifedipine significantly reduced systemic vascular resistance the difference between the drugs was not significant. The heart rate was significantly increased by nifedipine but not by molsidomine. The ejection phase indices were all increased by molsidomine and the increment in the mean normalized systolic ejection rate was significantly greater than that due to nifedipine. The left ventricular end-systolic volume index decreased significantly after molsidomine but not nifedipine. Neither drug significantly affected left ventricular end diastolic volume index, stroke volume index, maximal rate of rise of left ventricular pressure or left ventricular stroke work index.

Adult↗

PubMed1988

A clinical angiographic study of the arterial blood supply to the sinus node.

We studied the arterial blood supply to the sinus node area in 309 consecutive patients undergoing coronary arteriography. Seventy-nine had had a previous myocardial infarction. In two who developed temporary sinus node dysfunction, the sinus node artery arose from the distal portion of a severely stenotic left circumflex coronary artery, but in 307 of the 309 patients the sinus node arteries themselves were free of atheroma. The sinus node artery arose from the right coronary artery in 182 patients, from the proximal 3 cm in 179, near the origin of the acute marginal in one, and left of the crux in two. In 119 patients it arose from the left circumflex coronary artery, proximally in 87, and in 32 from anywhere throughout its length, running posteriorly as the posterior sinus node artery. Finally, eight patients had two sinus node arteries, one arising from the right coronary artery and one from the left circumflex.

Adult↗

PubMed1986

Rupture of the pericardium presenting as postpericardial trauma syndrome late after blunt chest injury.

A 40-year-old man presented with a clinical picture of postpericardial trauma syndrome six weeks after blunt injury to the chest. Posttraumatic pericardial rupture was diagnosed at exploratory thoracotomy. The presence of aortic regurgitation due to a previously undiagnosed congenital sinus of Valsalva aneurysm complicated the clinical picture. To our knowledge this is the first report of postpericardial trauma syndrome associated with pericardial rupture after blunt chest injury. It emphasizes the high index of suspicion required for diagnosis of pericardial rupture, a condition with potentially lethal complications.

Adult↗

PubMed1984

Cardiac arrhythmias in chronic renal failure? Holter monitoring during dialysis and everyday activity at home.

25 patients undergoing regular haemodialysis for chronic renal failure underwent Holter ECG monitoring for a continuous 48-hour period covering dialysis and the intermediate period of everyday activity at home. A low dialysate potassium concentration (1.7 mEq/l) was used. Clinically significant arrhythmias (greater than 100 ventricular extrasystoles/24 h) were found in only 1 patient and there were no complex ventricular arrhythmias. Benign atrial arrhythmias occurred in 22 patients (88%). Haemodialysis had no influence on type or frequency of arrhythmias.

Adolescent↗

PubMed1978

Contrast media during coronary arteriography: electrocardiographic changes in the presence of normal coronary arteries.

In forty patients with normal coronary arteries, the electrocardiographic changes secondary to Urografin 76 and Hypaque 85 injection into both coronary arteries were monitored. Hypaque caused significantly greater prolongation of the PR interval (p less than 0.001), depression of the ST segment (p less than 0.05) and depth of T wave inversion (p less than 0.05). These effects were more noticeable during right coronary artery injection. Both contrast media slowed the heart rate equally during right and left coronary artery injection. In the absence of coronary arterial disease the ECG changes secondary to contrast media injection probably reflect a direct toxic effect. It is possible that premedication with atropine will reduce these effects. Urografin 76 appears the less toxic of the two media, although one case of ventricular fibrillation occurred with each.

Angiocardiography↗

PubMedDate not supplied

Left atrial mechanical function in the healthy elderly: new insights from a combined assessment of changes in atrial volume and transmitral flow velocity.

To assess left atrial mechanical function in the elderly, 35 old (age > 70 years) and 18 sex-matched young (age < 50 years) healthy subjects were studied. Transmitral flow velocities were recorded with pulsed Doppler echocardiography. Left atrial volumes were measured echocardiographically at mitral valve opening (maximal) and closure (minimal) and at onset of atrial systole (P wave of the electrocardiogram) according to the biplane area-length method. Left atrial passive emptying was assessed with the passive emptying volume (maximal-volume at onset of atrial systole) and fraction (passive emptying volume/maximal). Left atrial active emptying was assessed with the active emptying volume (volume at onset of atrial systole-minimal) and fraction (active emptying volume/volume at onset of atrial systole) and with left atrial ejection force = 0.5.blood density.volume at onset of atrial systole.active emptying fraction.(A velocity)2/A integral. Left atrial volumes were greater in old compared with young subjects (maximal: 31 +/- 10 cm3/m2 vs 24 +/- 8 cm3/m2, p = 0.02; at onset of atrial systole: 23 +/- 8 cm3/m2 vs 15 +/- 5 cm3/m2, p = 0.0002; minimal: 13 +/- 5 cm3/m2 vs 9 +/- 4 cm3/m2, p = 0.001). Passive emptying volume and fraction were lower (7.8 +/- 1.7 cm3/m2 vs 9.2 +/- 3.2 cm3/m2 [p = 0.04] and 26.4% +/- 9.8% vs 37.9% +/- 11.2% [p = 0.003], respectively), whereas atrial ejection force and active emptying volume were greater in old compared with young subjects (6.8 +/- 3.3 kdynes/m2 vs 4.2 +/- 2.8 kdynes/m2 [p = 0.007] and 9.2 +/- 4.1 cm3/m2 vs 5.7 +/- 2.9 cm3/m2 [p = 0.002], respectively). The active emptying fraction was similar in the two groups (39.7% +/- 11% vs 38.4% +/- 13%; difference not significant). Thus advanced age is associated with depressed left atrial passive emptying function and increased left atrial volume. Left atrial dilation contributes to an increase in atrial ejection force and the amount of blood ejected during left atrial systole and may represent an important compensatory mechanism in this age population.

Adult↗

PubMedDate not supplied

Sinus node dysfunction in acute inferior myocardial infarction. Role of sinus node artery and clinical course in patients with one-vessel coronary artery disease.

To determine the role of the sinus node artery and the clinical course in postmyocardial infarction sinus node dysfunction, 27 patients with acute inferior myocardial infarction and single-vessel coronary artery disease were studied. In 13 patients (group 1) the infarct-related coronary artery was occluded proximally and in 14 (group 2) distally to the site of origin of the sinus node artery. At electrophysiology, performed 10 +/- 3 days from the acute event, basal and intrinsic heart rate were lower in group 1 compared to group 2 patients (54 +/- 4.8 vs. 69 +/- 7 beats/min, p = 0.001, and 66 +/- 7 vs. 76 +/- 8 beats/min, p = 0.006, respectively) while basal and intrinsic corrected sinus node recovery times were prolonged in group 1 compared to group 2 patients (585 +/- 49.3 vs. 324 +/- 61.3 ms, p = 0.0001, and 601 +/- 39.1 vs. 335 +/- 73 ms, p = 0.0001). During a 6-month follow-up no episodes of dizziness, syncope or angina were reported. Moreover, at the end of follow-up resting heart rate (70 +/- 11 vs. 73 +/- 7 beats/min, nonsignificant), maximal exercise heart rate (166 +/- 19 vs. 170 +/- 23 beats/min, nonsignificant), and exercise time (491 +/- 120 vs. 480 +/- 155 s, nonsignificant) were similar between the two groups and no exercise-induced ischemic ST segment depression was observed. Sinus node dysfunction in patients with inferior myocardial infarction and one-vessel disease is related to the occlusion of the infarct-related coronary artery proximal to the site of origin of the sinus node artery and is not associated with increased cardiovascular morbidity in the first 6 months from the acute event.

Adult↗

PubMedDate not supplied

The effects of enalapril on p53 expression in left ventricular cardiomyocytes after aortic stenosis.

ACE-inhibitors prevent the development of left ventricular hypertrophy (LVH). The tumor suppressor gene p53 up-regulates the cellular renin-angiotensin system, resulting in ANG II synthesis, which activates p53 creating a positive feedback loop. One hundred and fourteen rabbits were separated into groups A (control), B (sham-operated), C and D. In groups C and D, an aortic stenosis was performed, and in group D the animals were treated with enalapril. For p53 determination, LV specimens were examined by Western blot analysis and an immunohistochemical study was performed, except for samples from group D. In conclusion, LVH was significantly induced at 7 and 28 days after aortic stenosis with no difference between the two periods, while enalapril prevented hypertrophy in these two groups. p53 was transcriptionally activated and immunoreactively present after acute pressure overload as well as in the sham-operated group. Enalapril decreased the p53 expression at 180 min, 7 and 28 days following aortic stenosis.

Angiotensin-Converting Enzyme Inhibitors↗