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A Krupienicz

Publications and source records attributed to A Krupienicz.

14 recordsLinked to original sources

[Pseudoaneurysm of both superficial femoral arteries complicating coronary angiography: case report].

A 58 years-old patient with aortic valve disease was admitted to our hospital for coronarography. Coronarography by transfemoral route bilaterally failed and eventually the coronary arteries were visualised by the transaxillary route. After the study bilateral pseudoaneurysms of the superficial femoral arteries were diagnosed clinically and confirmed by color-Doppler and angiographic studies. Surgical therapy was successful. Causes, nature, diagnosis and surgical as well as nonsurgical therapy of the femoral artery pseudoaneurysms complicating percutaneous transfemoral cardiac catheterization are discussed.

Aneurysm

[Coexistence of WPW syndrome, coronary disease and segmental disorders of myocardial contraction. Diagnostic difficulties. Description of a case].

A 61 years old patient with Wolff-Parkinson-White's syndrome, and hypertension was admitted to the CCU, because of the first episode of substernal chest pain. ECG was deformed by Wolff-Parkinson-White's syndrome, type B, with accessory pathway located on the right side, without evolution. Serum enzymes remained low. Echocardiography showed akinesis of the posterior wall and hypokinesis of the lateral wall (the same contraction disorders were described in previous echocardiographical examination 5 years ago), it was observed that the first portion of myocardium to contract was the base of the right ventricle. To elucidate the etiology of the contraction disorders, scintigraphy of the heart, using Thallium 201, was performed, showing normal perfusion of the myocardium. To illustrate the dependence of the contraction disorders and abnormal depolarization pattern of the heart, echocardiographical examination was repeated, confirming the previous results, then 100 mg of Ajmaline was given to the patient intravenously, and echocardiographical examination was continued. Administration of the drug caused antidromic atrioventricular re-entrant tachycardia during which the lateral wall of the heart had been contracting properly. This case shows contraction disorders of the heart caused by the abnormal depolarization pattern, resulting from the presence of accessory pathway. It also illustrates the diagnostic difficulties in patients with Wolff-Parkinson-White's syndrome and suspected myocardial infarction, at the same time showing that scintigraphy of the heart might be very helpful in such patients. This case confirms the usefulness of echocardiography for localization of the accessory pathway.

Coronary Disease

[Unexplained syncope. Likelihood of inducing sustained ventricular tachycardia with electrophysiologic examination].

In patients with unexplained syncope and documented nonsustained VT or complex premature ventricular beats indication for programmed ventricular stimulation (PVS) should be considered. However, the variables derived from noninvasive methods that predict diagnostic yield of PVS are incompletely defined. The purpose of this study was to elucidate the role of noninvasive testing variables in predicting inducible monomorphic sustained ventricular tachycardia (SVT) in 116 patients (pts) presenting with syncope. The study group consisted of 45 pts with remote Q wave myocardial infarction. 5 pts with non-Q wave myocardial infarction, 21 pts with another heart disease and 45 pts without organic heart disease. All pts underwent standard ECG, Holter monitoring, echocardiography, signal-averaged ECG and PVS with 1, 2 and 3 extrastimuli at three basic cycle lengths. Nonsustained VT, low ejection fraction, prolongation of QTc interval, abnormal Q waves in postinfarction pts (Q-MI) and late potentials (LP) indicate a greatly increased probability of inducible SVT. Inducible SVT was present in 15 of 45 (33%) pts with Q-MI. Although in the group of 71 pts without Q-MI, nonsustained VT on Holter monitoring was detected in 20 pts, LP in 16 pts, prolongation of QTc interval in 3 pts and low ejection fraction in 2 pts, the positive yield of PVS was documented in only one case (1%). The combination of Q-MI and LP best predicted inducible SVT showing a sensitivity of 75%, specificity of 93%, overall predictive accuracy of 91%, predictive value of positive response of 63% and negative response of 69% to identify pts who would have inducible SVT. Thus, the combination of Q-MI and LP variables was shown as the best predictor of inducible SVT in pts with unexplained syncope. In pts without Q-MI the noninvasive testing variables have considerably less value in selection of pts to PVS, because inducible SVT is very rare in this population.

Adult

[Paroxysmal loss of consciousness. Comparison of electrophysiologic and holter monitoring results].

Holter monitoring is one of the most commonly done test in the evaluation of patients with syncope. As Holter monitoring may miss an arrhythmia or document an asymptomatic arrhythmia invasive electrophysiologic testing has been applied in patients with syncope. The purpose of this study was to compare Holter monitoring and electrophysiologic tests in patients with syncope of unexplained origin. The group consisted of 100 patients with syncope of unknown origin. Coronary artery disease was present in 43 patients, other heart disease in 19 patients and no structural heart disease was found in 38 patients. Electrophysiological testing consisted of (1) recording of His bundle electrogram, (2) atrial stimulation, (3) ventricular stimulation with 1.2 and 3 extrastimuli at three basic cycle lengths. The results of Holter monitoring were classified by severity of abnormalities into three classes: I--normal study; II--moderate abnormalities; III--severe abnormalities: sinus rhythm with pauses longer than 3 s, Mobitz II or complete atrio-ventricular block, supraventricular arrhythmia faster than 180 bpm, sustained ventricular tachycardia. Abnormalities of electrophysiologic testing were grouped as: I normal study; II--moderate abnormalities; III--severe abnormalities: sinus nodal recovery time more than 3 s, HV interval longer than 100 ms, supraventricular arrhythmia faster than 200 bpm, sustained ventricular tachycardia. Class III abnormalities were documented in 17 patients on Holter monitoring and in 20 patients by electrophysiologic testing. Compatibility between class III abnormalities in Holter monitoring and electrophysiological testing was noted in 4 patients, discordance of class III results in 33 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Relationship between QT interval duration and electrical induction of ventricular tachycardia.

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QTc) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 +/- 26 vs 396 +/- 19 ms, P less than 0.01), of 500 ms (407 +/- 20 vs 383 +/- 21 ms, P less than 0.01), and of 400 ms (390 +/- 21 vs 362 +/- 17 ms, P less than 0.001). During sinus rhythm the mean values of QTc were similar in both groups (408 +/- 25 vs 413 +/- 20 ms, NS). During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P less than 0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P less than 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.

Cardiac Pacing, Artificial

[Late ventricular potentials and spontaneous and electric stimulation-induced ventricular tachycardia].

The purpose of this study was to compare the relation of signal averaged variables of the QRS complex to spontaneous and to inducible sustained ventricular tachycardia. Signal averaging of the surface QRS complex was performed in 96 patients with coronary artery disease and ventricular arrhythmias. Twenty eight of them were evaluated by programmed electrical stimulation. Signal average variables were considered abnormal as: 1) the QRS duration as the time from the onset to end point of the QRS vector complex greater than 120 ms, 2) the maximal amplitude of the terminal 40 ms of the QRS vector complex less than 25 microV, 3) the duration of low (less than 40 microV) amplitude signal of QRS vector complex less than or equal to 40 ms. The ventricular late potentials were defined as the pressure of 2 or 3 abnormal averaged variables. Programmed electrical stimulation was performed using single and double extrastimuli at sinus rhythm and at ventricular pacing rates 100, 120, 140 bpm, followed by ventricular burst pacing (3 and 10 consecutive beats) at sinus rhythm. If stimulation of the right ventricular apex did not initiate ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation or two repetitive nonsustained ventricular tachycardias) right ventricular outflow tract stimulation was performed. Sustained ventricular tachycardia was defined as ventricular tachycardia lasting 30 s or requiring termination because hemodynamic compromise. Quantitative comparison of signal averaged variables was performed in patients with inducible versus noninducible ventricular tachycardia and in patients with spontaneous versus non-spontaneous ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials

[Comparative evaluation of the results of Holter monitoring and programmed ventricular stimulation in patients with ischemic heart disease].

24-hour ECG Holter monitoring and programmed ventricular stimulation were performed in 81 patients (64 males and 17 females aged 35-65). No ++anti-arrhythythmic agents nor beta-blockers were administrated. 58 patients suffered from myocardial infarction in the past, and 38 had a history of ventricular tachycardia. Right atrial and ventricular stimulation (in 7 patients also left ventricular stimulation) was performed using stimuli of a 2 ms pulse width. 24-hour ECG Holter monitoring was recorded on a magnetic tape from two bipolar precordial leads. Both examinations results were compared to assess correlation between ECG Holter monitoring parameters and inducibility of VT or VF by programmed stimulation. Significant correlation was stated among occurrence of: 1) spontaneous sustained ventricular tachycardia and induced by stimulation monomorphic sustained VT (p less than 0.005) as well as estimated both sustained and nonsustained VT (p less than 0.010) 2) spontaneous nonsustained VT and induced by stimulation sustained or nonsustained monomorphic VT (p less than 0.025). There was no correlation between spontaneous ventricular arrhythmias estimated by Lown and Wolf's classification and possibility to induce monomorphic VT as well as between any of ECG Holter monitoring parameters and polymorphic VT or ventricular fibrillation induced by stimulation. Aggressiveness extent of stimulation protocol necessary to induce monomorphic VT was similar in patients with or without VT recorded by Holter method.

Adult

Increased numbers of spleen colony forming units in B cell deficient CBA/N mice.

The formation of exogenous and endogenous spleen colonies was studied in immune-defective mice expressing the CBA/N X-linked xid gene. Bone marrow and spleen cells of immune deficient mice formed increased numbers of eight-day exogenous spleen colonies when transferred to either normal or B cell deficient lethally irradiated recipients. Moreover, defective mice showed increased formation of five-day endogenous spleen colonies (derived from transient endogenous colony forming units; T-CFU) and of ten-day endogenous spleen colonies (derived from CFU-S). Among the possible mechanisms responsible for the observed effects, the most probable appears the one in which decreased numbers of B cell precursors stimulate stem cell pools through a feedback mechanism.

Animals

[Tachycardiomyopathy].

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Cardiomyopathies