[The superior vena cava syndrome as a manifestation of dissection of the ascending aorta]. / Sindrom gornje suplje vene kao manifestacija disekcije ascendentne aorte.

INTRODUCTION: Most clinical manifestations of aortic dissection are due to complications of either ischemic origin or wall rupture of pleural, pericardial, peritoneal or mediastinal cavity. Compression of other blood vessels such as pulmonary artery or superior vena cava is possible, but rarely occurs. CASE REPORT: A 60 year-old patient was admitted to hospital due to severe cyanosis and edema of the face, neck and upper thorax. Ten years ago, due to aortic insufficiency, aortic valve replacement with mechanical prosthesis (St. Jude) was performed. Diagnosis of superior vena cava syndrome was established on the basis of clinical examination, ECG and chest radiography. The etiology was confirmed by echocardiography indicating an enormous dissecting aneurysm of the ascending aorta, 9.2 cm in diameter. Lethal outcome followed 24 h after admission according to the type of electromechanical dissociation. DISCUSSION: The first case of superior vena cava syndrome was described by William Hunter in 1757. This severe disease is caused by tumors which compress or develop inside superior vena cava. In cases of rapid symptom occurrence, thrombosis or compression of vena due to hematoma (trauma, voluminous, dissecting aortic aneurysm) should be considered. Since symptoms of aortic dissection were absent (thoracic pain, aortic regurgitation, pulse asymmetry) the etiologic diagnosis of superior vena cava syndrome was confirmed by echocardiography. Surgical treatment of dissection provides repermeabilization of the superior vena cava and loss of symptoms. CONCLUSION: Superior vena cava syndrome is a rare and slightly known clinical manifestation of ascending aortic dissection. If symptoms rapidly occur, dissection should be considered, particularly in previously surgically treated patients.

[The first non-Q myocardial infarct as a clinical manifestationn of acute coronary syndrome]. / Prvi non-Q infarkt miokarda kao klinicka manifestacija akutnog koronarnog sindroma.

INTRODUCTION: Non-Q myocardial infarction is only one of the possible clinical manifestations of acute coronary syndromes. Acute coronary syndrome is the most frequent cause of hospitalization in everyday cardiological practice. OBJECTIVES: 1. To evaluate the incidence of unstable angina and myocardial infarction in the group of patients admitted to hospital with diagnosis of acute coronary syndromes; 2. To evaluate the incidence of non-Q myocardial infarction in the group with index myocardial infarction; 3. To determine the frequency of different ECG changes in the subgroup with non-Q myocardial infarction. MATERIAL AND METHODS: The study was conducted at the Institute of Cardiovascular Diseases in Sremska Kamenica in the period between Jan. 1, 1997 and Dec. 31, 1999. Hospitalized patients with acute coronary syndromes (n = 3.337) were divided into subgroups with unstable angina (chest pain, ECG changes and normal level of CK) and with myocardial infarction (chest pain, ECG with/without changes, elevation of cardiac enzymes). Myocardial infarction without Q waves on ECG was considered to be non-Q myocardial infarction. Initial ECG changes (ST elevation, ST depression, inverted T waves, abscence of changes) were evaluated in patients with non-Q myocardial infarction who were not treated with Streptase. RESULTS: During a three-year period, 3.337 patients with acute coronary syndrome were hospitalized. 65.3% of them had unstable angina, while 34.7% suffered from myocardial infarction. In the group with myocardial infarction, 12.9% (280/2179) had reinfarction. 8.8% of patients were treated with thrombolytic agents, which prevented formation of Q waves in 24.6% of patients. In the group of patients who were not treated with thrombolytics, 196 patients (11.8%) fulfilled criteria for non-Q myocardial infarction. Incidence of initial ST elevation, ST depression and inverted T waves in those patients with non-Q myocardial infarction were 11.2%, 35.2% and 52.1% respectively, whereas 1.5% had no ECG changes. CONCLUSION: Both incidence of unstable angina and non-Q myocardial infarction, as manifestations of acute coronary syndromes, and incidence of newly formed ST elevation, which is one of the forms of initial ECG changes in non-Q myocardial infarction, are significantly lower than those found in literature.

Direct intracoronary stent implantation.

The standard stent implantation technique requires routine predilatation of the target lesion with balloon catheter. Since occurrence of complications is possible, direct stent implantation without previous dilatation has been performed recently. In this study, a complex case of coronary lesion treated with direct stent implantation in a patient with unstable angina after diaphragmal myocardial infarction was reported. A coronary angiography finding indicated presence of severe eccentric stenosis in the proximal third of the dominant right coronary artery. The system of the left coronary artery was without stenotic lesions. After antiaggregation combination of aspirin and ticlopidine, the stent was successfully implanted and dilated under the pressure of 14 atmospheres. The control coronary angiography did not show residual stenosis of the right coronary artery. The patient was discharged without subjective discomforts for further out-patient treatment.

[Relation between mitral orifice surface area and extent of hemodynamic disorder of the pulmonary circulation in patients with mitral stenosis]. / Odnos izmedu povrsine mitralnog usca i stepena hemodinamickih poremecaja u plucnoj cirkulaciji kod bolesnika s mitralnom stenozom.

UNLABELLED: Mitral annulus and valves form the mitral orifice area with the size between 4.0-6.0 cm2. Every area which is smaller than this, represents mitral stenosis. As a consequence of mitral stenosis hemodynamic gradients occur over the mitral orifice with circulation disturbances below and above the stenotic mitral valve. The size of transmitral gradient is important in the evaluation of functional or/and structural changes in the blood vessels of pulmonary circulation. This investigation included 40 patients with mitral stenosis (or accompanying minimal mitral regurgitation). All patients underwent echocardiographic examination: area of the mitral orifice was determined and hemodynamic procedure with the left and right heart catheterization was performed. The following hemodynamic parameters were measured: mean capillary wedge pressure, left ventricular filling pressure, left ventricular mean diastolic pressure, mean pulmonary artery pressure. According to these parameters resistance in the pulmonary circulation was measured. The size of the mitral orifice was determined according to oximetry blood analyses and hemodynamic parameters. All patients were divided into 4 groups: minimal (2.5-4.0 cm2), mild (1.5-2.5 cm2), moderate (1.0-1.5 cm2) and severe mitral stenosis (1.0 cm2). The comparison of echocardiographic and hemodynamic parameters revealed a high and positive correlation between the area of mitral orifice. There was also a negative and moderate correlation between the values of stenotic mitral orifice area and total pulmonary resistance, i.e. in all patients with severe mitral stenosis there was an increased pulmonary arteriolar resistance. CONCLUSION: Noninvasive echocardiographic method is valid in the evaluation of stenotic mitral valve area. In the evaluation of hemodynamic parameters in the pulmonary circulation the index of arteriolar pulmonary systemic vascular resistance is very important. In all patients with the area of stenotic mitral orifice 1.0 cm2, there are functional or pathomorphologic changes in the pulmonary circulation of the blood vessel wall.

[Angiographically tight coronary stenoses without transstenotic pressure gradient]. / Sténoses coronaires angiographiquement serrées sans gradient de pression transsténotique.

The availability of coronary angioplasty catheters has made it possible to measure transstenotic pressure gradients. This parameter provides direct information on coronary haemodynamics. In 2 patients with proximal concentric stenosis of the left anterior descending artery the gradient was zero in spite of a more than 50% reduction in vascular diameter. The reason for this emerged from a study of the characteristics of these stenoses: they were short, and the vascular area at their level clearly was superior to 1 mm2. None of the 2 patients suffered from angina. One had negative exercise ECG, the other had an inconclusive exercise test without pain but with ST segment depression on anterior leads. This patient had a history of posterior infarction with postero-inferior dyskinesia at angiography, and exercise scintigraphy with thallium showed no decreased uptake in the antero-septal territory. The presence of coronary transstenotic pressure gradient implies a fall in coronary blood pressure downstream of the stenosis, a pressure which constitutes the perfusion pressure in the territory fed by the narrowed artery. on the value of this perfusion pressure depends the possibility of coronary blood flow autoregulation in the territory threatened by ischaemia.