1/9. An adult case with an abnormal right ventricular structure causing intraventricular pressure gradient and a history of aphthous stomatitis and thrombophlebitis.We report a 50-year-old man with a right ventricular structure causing an intraventricular pressure gradient. He had been diagnosed as vasculo-Behcet with a history of aphthous stomatitis and thrombophlebitis. He had also been suffering from atrial flutter and mild right-side heart failure. echocardiography showed that there was an abnormal structure attached to the right ventricular free wall and protruding into the cavity, and that it caused the pressure gradient estimated to be approximately 19 mmHg. Chest X-ray computed tomography demonstrated that the structure was partially calcified. magnetic resonance imaging depicted the structure separating the right ventricle into two chambers. Angiographic study revealed a markedly enlarged right atrium and a filling defect at the mid-portion of the right ventricle, which divided the right ventricular cavity into two parts. Hemodynamic study showed a slightly elevated right atrial pressure (mean 7 mmHg) and a peak-to-peak intraventricular pressure difference of 18 mmHg in the right ventricle. The diastolic pressure tracing of the right ventricular low pressure chamber showed a 'dip and plateau' pattern. Although the pathological features of the abnormal right ventricular structure in this case were not fully clarified, abnormal muscle bundle and/or endocardial fibrosis, which were reported to be associated with Behcet's disease, may have contributed to its generation.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/9. Surgical treatment of tricuspid regurgitation caused by Loffler's endocarditis.A 25-year-old man with a history of bone-marrow-transplantation for the treatment of Loffler's endocarditis underwent surgery for massive tricuspid regurgitation with paroxysmal atrial flutter. Dense fibrosis in the right ventricular endocardium with complete obliteration of the apex was seen intraoperatively, and the right ventricular cavity was diminished. Annular dilatation of the tricuspid valve and entrapment of the posterior leaflet to the endocardial fibrosis were also seen. Annuloplication at the posterior leaflet was performed. In addition, the right atrial free wall was widely resected and the septal and inferior vena cava-tricuspid valve isthmi were cryoablated for the treatment of atrial flutter. Postoperative catheterization revealed rather high right ventricular end-diastolic pressure. However, tricuspid regurgitation disappeared with the increased cardiac output. atrial flutter could not be induced by repetitive stimulation in the postoperative electrophysiological examination.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
3/9. Apical hypertrophic cardiomyopathy associated with life-threatening paroxysmal atrial flutter with a slow ventricular response: a case report.A 58-year-old male patient had apical hypertrophic cardiomyopathy (HCM) associated with a life-threatening tachycardia due to atrial flutter. Following palpitation and dyspnea for 2-3 h, he became unconscious because of circulatory catastrophe, but was fully resuscitated. An electrocardiogram recorded just before the loss of consciousness revealed atrial flutter at a rate of 260 beats/min with a 2:1 ventricular response. He was diagnosed as having apical HCM based on the echocardiographic and left ventriculographic findings. Atrial stimulation at a rate of 150 pacings/min for 1 min caused a marked drop in systemic systolic blood pressure from 170 to 120 mmHg. The patient was treated with 150 mg of cibenzoline per day to prevent supraventricular tachyarrhythmias and to improve left ventricular diastolic function. At the time of the recent follow-up at 2 and a half years, he felt quite well.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
4/9. Altered dystrophin expression in the right atrium of a patient after fontan procedure with atrial flutter.Underlying mechanisms in the development of atrial flutter or intra-atrial re-entry tachycardia in patients with structural cardiac abnormalities remain poorly defined. The right atrial myocardium from two patients with congenital heart disease was evaluated, of whom one presented with severe right atrial dilation and arrhythmia and the other with a normal right atrium, to assess whether increased right atrial pressure and volume overload give rise to sarcolemmal alteration. N-terminus dystrophin staining in the atrium from the patient who had undergone a fontan procedure showed a normally distributed but significantly reduced staining signal compared with the second patient. This is the first report that patients with severe right atrial dilation and atrial flutter have marked reduction in atrial dystrophin expression.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
5/9. Left ventricular hypertrabeculation/noncompaction as a cardiac manifestation of Duchenne muscular dystrophy under non-invasive positive-pressure ventilation.Though cardiac involvement is a frequent finding in patients with Duchenne muscular dystrophy (DMD) at the wheel-chair-bound stage, left ventricular hypertrabeculation (LVHT) has not been reported. The patient is a 28-year-old male with the typical clinical features of end stage DMD. Since the age of 16 years he required ventilatory support by means of non-invasive positive-pressure ventilation (NIPPV), initially intermittently and since age 27 permanently. Since the age of 21 years he developed chronic heart failure, and since age 24 atrial flutter, successfully treated with amiodarone. After discontinuation of amiodarone because of hyperthyroidism, he developed atrial fibrillation. echocardiography at age 28 revealed mitral insufficiency, enlarged left atrial diameter, and, surprisingly, LVHT. Since LVHT was absent at the initial echocardiographic examination, it was regarded acquired. The case shows that cardiac involvement in DMD may not only comprise rhythm abnormalities, valve abnormalities, and dilative cardiomyopathy, but also LVHT in single cases.- - - - - - - - - - ranking = 0.5keywords = pressure (Clic here for more details about this article) |
6/9. The mechanism of flutter interval alternans.The mechanism of atrial flutter alternans was investigated by observing the effects of ventricular systole on flutter intervals in a patient with atrioventricular dissociation. Interval measurements were made both from atrial electrograms recorded from an esophageal electrode, and from surface ECG recordings. Flutter cycle intervals that occurred during a well-defined period subsequent to ventricular systole were consistently prolonged by up to 30 msec relative to the baseline flutter cycle interval. This prolongation was observed in two vastly different electrode configurations, implying that motion artifact was not predominantly responsible. We concluded that, by altering the characteristics of the flutter reentry circuit, transient increases in atrial volume and/or pressure arising during ventricular systole were responsible for the lengthening of the flutter cycle intervals.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
7/9. Electrocardiographically discrete right and left ventricular QRS complexes: a case report.A patient with congestive cardiomyopathy manifested a right ventricular QRS followed after 80 msec. by a left ventricular QRS in response to a single atrial depolarization. The ventricular sequence was reversible when the left ventricle was paced directly. Virtually the entire ipsilateral ventricular ejection period occurred during diastolic filling of the contralateral ventricle. Triggered left ventricular pacing, using the right ventricular electrogram as trigger, shortened the QRSRV-QRSLV interval and resulted in a reduction of left ventricular filling pressure and a significant rise in cardiac output. These findings indicated an independent contribution of this unique form of interventricular conduction disturbance to deterioration in hemodynamic performance.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
8/9. atrial flutter with exit block.The mechanism of atrial flutter is controversial. A 76-year-old woman with rheumatic heart disease was referred to our clinic with an unusual rhythm disturbance which initially appeared to be classic atrial flutter at a rate of 300 beats/min. Later tracings, however, demonstrated a rate exactly one-half that of the earlier ECGs, with an identical p-wave morphology and vector. This latter rhythm also behaved in a manner expected for a flutter mechanism in that both spontaneously and with carotid pressure high-degree atrioventricular block occurred without alteration of the underlying atrial mechanism. Finally, the two rates interchanged spontaneously over several days without any significant interval changes in medical therapy. These findings were initially explained as probable digoxin toxicity. The underlying mechanism, however, was more likely atrial flutter with exit block and in this patient may have represented another facet of her sick sinus syndrome. This unusual phenomenon is discussed in terms of previous reports and possible implications for the mechanism of atrial flutter.- - - - - - - - - - ranking = 0.1keywords = pressure (Clic here for more details about this article) |
9/9. Supraventricular arrhythmia as the cause of sudden death in hypertrophic cardiomyopathy.Electrophysiological studies with simultaneous echocardiographic control and invasive measurement of intravascular pressures were carried out in a 13-year-old boy with hypertrophic cardiomyopathy who was hospitalized after an episode of aborted sudden death. Ventricular stimulation did not induce ventricular tachycardia, but atrial stimulation induced atrial fibrillation, atrial flutter and non-sustained ventricular tachycardia. Atrial stimulation (S1) at 200 beats.min-1 (10-15 s) also induced significant repolarization abnormalities in the 5-10 post-stimulation beats. Akinesia of the ventricular septum and posterior wall without opening of the mitral valve was documented by echocardiography. A complete anterior systolic motion, not observed under basal conditions, was detected in the first post-stimulation beat. Atrial stimulation at rates over 120 beats.min-1 caused a drop in systolic blood pressure, a rise in pulmonary artery pressure, and a decrease in cardiac output. Despite therapy with propranolol and amiodarone, the patient died suddenly.- - - - - - - - - - ranking = 0.3keywords = pressure (Clic here for more details about this article) |