Impending paradoxic embolism resolved by intravenous heparin administration.
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Biomedical subjects
Publications and source records attributed to M Csanády.
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BACKGROUND: Echocardiographic parameters for predicting cardioversion outcome in patients with non-valvular atrial fibrillation are not accurately defined. OBJECTIVE: To evaluate the role of left atrial appendage flow velocity detected by transoesophageal echocardiography for prediction of cardioversion outcome in patients with non-valvular atrial fibrillation enrolled in a prospective. multicentre, international study. METHODS: Four hundred and eight patients (257 males, mean age: 66 +/- 10 years) with non-valvular atrial fibrillation lasting more than 48 h but less than 1 year underwent transthoracic echocardiography and transoesophageal echocardiography before either electrical (n=324) or pharmacological (n=84) cardioversion. RESULTS: Cardioversion was successful in restoring sinus rhythm in 328 (80%) and unsuccessful in 80 patients (20%). Mean left atrial appendage peak emptying flow velocity was significantly higher in patients with successful than in those with unsuccessful cardioversion (32.4 +/- 17.7 vs 23.5 +/- 13.6 cm x s(-1); P<0.0001). At multivariate logistic regression analysis, three parameters proved to be independent predictors of cardioversion success: the atrial fibrillation duration <2 weeks (P=0.011, OR=4.9, CI 95%=1.9-12.7), the mean left atrial appendage flow velocity >31 cm x s(-1) (P=0.0013, OR=2.8, CI 95%=1.5-5.4) and the left atrial diameter <47 mm (P=0.093, OR=2.0, CI 95%=1.2-3.4). These independent predictors of cardioversion success outperformed other univariate predictors such as left ventricular end-diastolic diameter <58 mm, ejection fraction >56% and the absence of left atrial spontaneous echo contrast. CONCLUSION: In patients with non-valvular atrial fibrillation, measurement of the left atrial appendage flow velocity profile by transoesophageal echocardiography before cardioversion provides valuable information for prediction of cardioversion outcome.
Baroreflex sensitivity (BRS) by the spontaneous sequence technique has been widely used as a cardiac autonomic index for a variety of pathological conditions. However, little information is available on determinants of the variability of spontaneous BRS and on age-related reference values of this measurement in a healthy population. We evaluated BRS as the slope of spontaneous changes in systolic blood pressure (BP) and pulse interval from 10 minutes BP (Finapres) and ECG recordings in 1134 healthy volunteers 18 to 60 years of age. Measurement of BRS could be obtained in 90% of subjects. Those with unmeasurable spontaneous BRS had a slightly lower heart rate but were otherwise not different from the rest of the population. BRS was inversely related to age (lnBRS, 3.24-0.03xage; r(2)=0.23; P:<0.0001) in both genders. In addition, univariate analysis revealed a significant inverse correlation between BRS and heart rate, body mass index, and BP. Sedentary lifestyle and regular alcohol consumption were also associated with lower BRS. However, only age, heart rate, systolic and diastolic BP, body mass index, smoking, and gender were independent predictors of BRS in a multivariate model, accounting for 47% of the variance of BRS. The present study provides reference values for spontaneous BRS in a healthy white population. Only approximately half of the variability of BRS could be explained by anthropometric variables and common risk factors, which suggests that a significant proportion of interindividual differences may reflect genetic heterogeneity.
The relationship between coronary flow reserve and the result of coronarography was examined. 152 patients were investigated by stress transoesophageal echocardiography and coronary angiography. The value of coronary flow reserve was significantly lower in cases of significant coronary stenosis than in those patients who had a normal coronarography (in patients with left anterior descending coronary artery stenosis: 1.77 +/- 0.47 vs in cases with normal coronary angiogram: 3.19 +/- 1.15). There was no difference in the value of CFR in those cases where not only LAD stenosis but CX or RC stenosis was also found. The value of coronary flow reserve was significantly higher in RC or CX patients than that of LAD patients. In patients with positive stress and negative coronarography (X syndrome) the coronary flow reserve was 1.23 +/- 0.2, which value was significantly lower as compared to patients with significant coronary stenosis.
The case history of a 49-year-old female patient is reported, who was operated on because of varicose vein in the left lower extremity. A few days after the operation serious signs of cerebrovascular insult appeared. The clinical picture and the result of an urgent transoesophageal echocardiography are described; a serpentine thrombus was found to be trapped in the patent foramen ovale. During continuous intravenous heparin treatment, the patient gradually recovered, but a residual neurological deficit could be detected on discharge from the hospital. Six days after the admission, repeated transoesophageal echocardiographic examination showed no signs of intracardiac thrombus. The clinical feature of the illness, the predisposing factors, the diagnostic and therapeutic possibilities are discussed.
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The long QT syndrome (LQTS) is a heart disorder which is characterised by the prolongation of the QT interval of the surface electrocardiogram and is associated with malignant arrhythmias, syncopal episodes, torsade de pointes form ventricular tachycardias and an increased risk of sudden cardiac death. There are two familial forms of LQTS, the autosomal dominant Romano-Ward syndrome and the autosomal recessive Jervell-Lange-Nielsen syndrome which is associated with congenital senzorineural deaf-mutism. Recent advances in molecular genetics have allowed to identify mutations in four genes, KvLQT1 (11p15.5), HERG (7q35), SCN5A (3p21) and minK (21q22), which cause LQTS. There is a fifth genetic locus known on chromosome 4 (4q25-27), where the disease causing gene has not been identified yet. As LQTS genes code proteins which form sodium and potassium channels of the heart, LQTS can be regarded as the disease of cardiac ion channels. The KvLQT1 and minK genes code the slowly activating, delayed rectifier (Iks) potassium channel, the HERG gene code the rapidly activating, delayed rectifier (Ikr) potassium channel of the heart, while the SCN5A gene codes a cardiac sodium channel. Mutations in KvLQT1, minK and HERG genes affects repolarising, rectifier potassium currents, while SCN5A mutations cause delayed inactivation and reopening of the cardiac sodium channel, which initiates the depolarisation of cardiac cells. Both alterations result in a prolongation of cardiac repolarisation which is represented in the elongation of the QT interval. Elucidation of the genetic base of the disease provided new tools in the clinical management of LQTS. It has been shown that changes in the repolarisation parameters on the ECG may be predictive for the causative gene and different LQTS genes are associated with different clinical picture. More importantly, it is possible to use "gene-specific" therapy in LQTS which specifically targets ion channels affected by given gene mutations.
Endoscopic CO(2) laser intervention can be used as conservation surgery for supraglottic laryngeal carcinomas in carefully selected patients. We analyzed retrospectively our experience in managing patients with early supraglottic carcinomas operated on at the Clinic of Otorhinolaryngology, Szeged, Hungary, during the 10-year period between 1987 and 1997. Conservation surgery was the treatment of choice in 187 patients, but only 23 (12%) were selected for endoscopic CO(2) laser surgery. Laser surgery was indicated predominantly for T1 cancer of the epiglottis (n = 15), but was also performed for T2 cancers (n = 8). Of the 23 supraglottic tumors treated, 16 had no signs of recurrence to date (1.5 to 9 years after surgery) a local control rate of 70%. Six patients with recurrences underwent salvage therapies that included repeated laser excisions (n = 3), radiotherapy (to 60 Gy), horizontal supraglottic laryngectomy and total laryngectomy. One patient was not resectable because of multiple metastases. Our experience with endolaryngeal CO(2) laser excision indicates that it is a reasonable method in selected cases of supraglottic tumors, but one-third of the patients required salvage treatment.
BACKGROUND: Several studies have demonstrated a consistently high sensitivity of dobutamine echocardiography whereas test specificity in these series has been variable. The aim of this study was to evaluate whether coronary vasospasm--elicited by alpha1 adrenoreceptor stimulation--may be a significant source of false positive responses during dobutamine stress. METHODS: From the data bank of four institutions we selected 113 patients (75 males, 38 females, mean age 55 +/- 12 years) with dobutamine echocardiography performed (up to 40 micrograms/kg/min and atropine 1 mg if needed) before a coronary angiography showing normal or near normal (visually assessed stenosis severity < 50%) coronary arteries. The following variables--which were previously reported influencing dobutamine echo specificity--entered the multivariate statistical analysis: age, sex, heart rate at baseline and at peak stress, baseline echo, hypertension, site of asynergy, and spasm at coronary angiography. RESULTS: Twenty-five patients had a positive dobutamine test. The positivity occurred in the left coronary territory in 15 and in the right coronary territory in 10 cases. All the 6 patients with spontaneous spasm during angiography had a false positive stress test result. By multivariate analysis only coronary artery spasm during angiography (p = 0.0015) and history of hypertension (p = 0.0031) were significant predictors of false positive results of dobutamine stress echocardiography. CONCLUSIONS: Coronary artery spasm may be an important source of false positive results during dobutamine stress echocardiography.
Recent developments in molecular genetics have allowed to identify mutations in seven genes coding the beta myosin heavy chain, troponin T, alpha tropomyosin, myosin binding protein C, essential and regulatory myosin light chains and troponin I causing hypertrophic cardiomyopathy. These mutations affect critical, evolutionary conserved nucleotides of these genes and influence vital functions of the encoded proteins. As all seven genes encodes sarcomeric proteins in the heart muscle, hypertrophic cardiomyopathy is regarded these days as a disease of the sarcomer. Recent data indicate that some mutations are associated with "malignant" clinical picture, with rapidly developing, severe symptoms of the disease and increased risk of sudden cardiac death while other mutations bear a more favourable prognosis. Apart of the disease causing mutation other factors, including disease modifier genes, are likely to make an impact on the clinical appearance of hypertrophic cardiomyopathy. The knowledge provided by molecular genetics influences the clinical management of the disease even today and based on the investigation of mutation carrying patients new diagnostic criteria was proposed for hypertrophic cardiomyopathy. The challenge for the future is the establishment of routine genetic diagnostics and the development of possible gene therapy.
We report on the case of a 45-year-old man with recurrent syncope and angina with shortness of breath on exertion. Invasive and noninvasive diagnostic methods revealed severely stenosed bicuspid aortic valve, postductal coarctation of the aorta, and a coronary artery-descending aorta fistula. After surgical correction of the coarctation, ligation of the fistula, and aortic valve replacement, the patient's symptoms resolved.
Under physiological conditions, the pancreas scarcely influences the function of the cardiovascular system, although the hormones produced in the healthy pancreas (insulin, glucagon and somatostatin) affect the myocardial contractility in pharmacological doses. Among the diseases of the pancreas, the pancreatic tumours (insulinoma, glucagonoma and vipoma), furthermore the acute and chronic pancreatitis involve cardiovascular complications, which influence the outcome of the disease. Although the clinical picture is dominated by the metabolic changes of the excessively produced hormones in pancreatic tumours, the cardiac and vascular effects of the hormones may be considerable. In acute necrotizing pancreatitis, enzymes released from the pancreas and inflammatory mediators transform acute necrotizing pancreatitis into "multiple organ disease"; one of the important forms of this disease is the cardiovascular shock syndrome. One of the best-known complications of chronic pancreatitis is the pancreoprive diabetes mellitus, and beside that other, nonspecific cardiac alterations (e.g. ECG-changes) may occur.
The objective of this study was to compare the baroreflex sensitivity (BRS) assessed by the new, non-invasive, spontaneous sequence method (BRS-sequence) with the Valsalva manoeuvrebased BRS. Fourteen healthy volunteers were studied in the supine position, during 60 degrees head-up tilt (HUT) and during -30 degrees head-down tilt (HDT). Blood pressure and R-R intervals were continuously and non-invasively recorded using a Finapres device. The BRS-sequence was assessed by analysing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and R-R interval of the following beat increased or decreased in the same direction in a linear fashion; it was compared with data obtained during the Valsalva manoeuvre in each position. The time and frequency domain indices of R-R interval variability were also evaluated. The mean difference of BRS between the two non-invasive methods was 3.86 ms/mmHg with a standard deviation of 9.14 ms/mmHg. BRS was decreased during HUT and increased during HDT as assessed by both techniques. The changes in BRS were associated with vagal withdrawal and sympathetic activation during HUT and enhancement in the cardiac vagal tone and reduction in the sympathetic activity during HDT. We conclude that the BRS-sequence technique provides a reliable method to study the neural control of the circulation, although the body position in consecutive measurements needs to be standardized.
Hemodynamic parameters of experimental acute necrotizing pancreatitis (AP) were monitored by means of echocardiography in rabbits. Left ventricular (LV) systolic and diastolic parameters were determined before and 1, 3, 6, 12, 18, and 24 hr after injection of taurocholic acid in the pancreatic duct in AP animals. Temporary LV dilatation was observed 6 hr after the AP induction [LV end-diastolic (ED) diameter from 1.16 +/- 0.04 to 1.22 +/- 0.04 cm, P < 0.05, ED volume from 2.98 +/- 0.34 to 3.57 +/- 0.75 ml, P < 0.05] without decrease in systolic function. Cardiac output (CO) and stroke volume (StV) was increased in both groups 3 hr after the operation (from 0.53 +/- 0.15 to 0.71 +/- 0.06 L/min, P < 0.05 in AP), but in the AP animals it remained high. However, 24 hr after AP induction, both the CO and the StV were decreased significantly. The LV diastolic function was impaired 1 hr after AP induction, but had recovered after 12 hr. In conclusion, an early diastolic impairment followed by LV enlargement could be noninvasively observed in experimental AP in rabbits.
Attainment of the regression of hypertension-associated left ventricular hypertrophy (LVH) seems to be a desirable goal of blood pressure (BP)-reducing therapy. Since antihypertensive drugs of differing types may exhibit markedly different abilities to modulate LVH, we examined the effects of the angiotensin-converting enzyme inhibitor cilazapril, and the potassium channel activator minoxidil, alone or in combination with each other, on the left ventricular mass (LVM) in patients with severe essential hypertension who had LVH detected by echocardiography. All patients received the same base therapy of bopindolol and guanfacine. After a run-in period, they were treated with: (1) cilazapril (n = 10); (2) minoxidil, combined with a diuretic (n = 10); or (3) both cilazapril and monoxidil (n = 6) for 12 months. The LVM index (LVMI; LVM per body surface area) was estimated every 3 months by means of echocardiography. Each kind of therapy decreased the arterial pressures to a similar degree. The 1-year treatment with the cilazapril-based regimen resulted in a significantly diminished LVMI (from a mean +/- s.d. of 173 +/- 38 to 152 +/- 22 g/m2; P < 0.05). On the other hand, the minoxidil-based therapy led to a significant increase in LVMI (from 148 +/- 19 to 170 +/- 35 g/m2; P < 0.05). There were no significant LVMI changes in patients receiving the combined, cilazapril + minoxidil-based treatment (172 +/- 34 vs the pretreatment 183 +/- 54 g/m2). The results confirm that long-term treatment with cilazapril is effective both in reducing BP and in reducing LVM. In spite of yielding a satisfactory reduction of BP, minoxidil therapy, even in combination with a diuretic and a beta-blocker, may lead to an aggravation of pre-existing LVH; this effect of minoxidil could be prevented by the simultaneous administration of cilazapril.
Numerous antihypertensive drugs exist with different modes of action, which have a really effective impact on hypertension. The life expectancy of hypertensive patients is known to depend on the degree of damage caused to their target organs by the hypertension itself. Cardiovascular hypertrophy and its complications are considered to be among the major elements of this process. This work evaluates the effectiveness of the long-term treatment of essential hypertensive subjects (n = 10) with a long-acting ACE-inhibitor, cilazapril, as concerns their blood pressure and cardiac hypertrophy. Cilazapril given orally in a daily dose of 2.5 mg effectively lowered both the systolic (delta 30 mm Hg) and the diastolic (delta 19 mm Hg) blood pressure. No changes were found in body weight or heart rate, and only one side-effects (skin rash) was reported. Cilazapril considerably decreased the left ventricular mass and hence the hypertrophic index of hypertensive patients with cardiac hypertrophy, suggesting that ACE inhibitors are effective not only in lowering blood pressure and decreasing hypertrophy, but also in lowering the cardiac morbidity and mortality.
1. A decreased heart period variability and baroreflex sensitivity in patients with acute myocardial infarction have already been documented. Since one of the major determinants of heart period variability is blood pressure variability, it would be important to know the characteristics of blood pressure regulation in this setting. The changes in blood pressure variability during the acute phase of myocardial infarction have not yet been studied. 2. We investigated the blood pressure variability and the heart period variability in 11 patients with acute myocardial infarction 3 to 5 days after their admission. Thirteen age matched patients with no evidence signs of ischaemic heart disease or previous myocardial infarction served as controls. We used the frequency domain indexes of short term measurements of finger blood pressure variability and heart period variability. The spectral powers for both heart period variability and blood pressure variability were divided into three major components: total frequency (0.01-0.4 Hz), low frequency (0.04-0.15 Hz) and high frequency (0.15-0.4 Hz). 3. All of the frequency-domain components of the heart period variability were significantly decreased in patients with recent acute myocardial infarction compared to the controls: Ln(total power): 5.68 +/- 0.24 vs. 7.21 +/- 0.29, Ln(low-frequency power): 4.31 +/- 0.28 vs. 7.05 +/- 0.53, Ln(high-frequency power): 3.50 +/- 0.33 vs. 5.48 +/- 0.32. Acute myocardial infarction patients showed a significantly reduced blood pressure variability in all frequency components compared to the controls: Ln(total power): 4.21 +/- 0.18 vs. 6.79 +/- 0.48, Ln(low-frequency power): 2.40 +/- 0.24 vs. 4.36 +/- 0.21, Ln(high-frequency power): 3.31 +/- 0.25 vs. 5.66 +/- 0.38. 4. We hypothesize that the reduced blood pressure variability in the acute phase of myocardial infarction could be related to a relative invariance of stroke volume. The underlying mechanism is the reduced left ventricular compliance.
OBJECTIVE: To determine cardiac manifestations in primary Sjögren's syndrome (SS). METHODS: Echocardiographic examination was undertaken in 64 patients (62 women, two men) with primary SS (54 definite (DSS) and 10 probable (PSS)) who had systemic symptoms. Twenty one healthy women volunteers of similar age acted as controls. RESULTS: Acute exudative pericarditis occurred in only one patient. An echogenic pericardium was demonstrated in 21 patients (19 DSS, two PSS) (33%) who had a previous symptom free pericarditis, but in none of the controls. Pulmonary pressure was significantly greater in the patients than in the controls (31 (SD 8) mm Hg compared with 24 (7) mm Hg), but there was no significant difference between the DSS and PSS groups. Left ventricular (LV) systolic function was similar in patients and controls. Twenty two patients (20 DSS, two PSS) and one control subject were excluded from LV diastolic function evaluation because of conditions likely to influence the parameters. Of the remaining 42 patients with SS (34 DSS, eight PSS), 21 (17 DSS, four PSS) had impaired diastolic function, confirmed by several diastolic parameters. LV diastolic dysfunction and echogenic pericardium occurred independently of each other, and there was no correlation between the occurrence of these silent cardiac abnormalities and the clinical and laboratory findings. CONCLUSIONS: Obvious cardiac involvement is rare in primary SS, but clinically silent manifestations (symptom free pericarditis and LV diastolic dysfunction) are common. The clinical and prognostic significance of these changes cannot yet be defined.