Ablation Approaches for Ventricular Fibrillation

Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in “curing” VF are proving to be life saving for resuscitated survivors of arrhythmic death.     

Cardiac autotransplantation for surgical resection of a primary malignant left ventricular tumor

Primary cardiac sarcomas are rare. In such tumors, surgical resection is sometimes considered necessary to correct obstruction of flow caused by the tumor and to accomplish complete resection. The anatomic difficulties associated with large, primary, intracavitary left-sided sarcomas have led us to use cardiac explantation, ex vivo tumor resection, and cardiac autotransplantation to meet the anatomic challenges of left atrial tumors. We report the case of a patient who had a large, primary, intracavitary, left ventricular sarcoma that was successfully removed by cardiac explantation and ex vivo reconstruction with use of the cardiac autotransplantation technique. This is the 1st report describing the use of cardiac autotransplantation to surgically resect an intracavitary left ventricular malignancy.     

Characterization of acute experimental left ventricular thrombi with quantitative backscatter imaging

Two-dimensional echocardiography is an excellent technique for detecting left ventricular thrombi, however, acute clot is sometimes difficult to differentiate from adjacent myocardium and intracavitary signals. We hypothesized that quantitative assessment of the acoustic properties of acute left ventricular thrombi using a quantitative backscatter imaging system would permit the differentiation of thrombus from adjacent myocardium and intracavitary echoes. Acute, experimental left ventricular thrombi in seven dogs were evaluated with a quantitative backscatter imaging system that allowed the measurement of relative integrated backscatter and cyclic (i.e., diastolic minus systolic) variation in integrated backscatter. Coronary ligation abolished the cyclic variation in relative backscatter that occurred in normal myocardium. The end-diastolic relative backscatter in the thrombus (16.9 +/- 1.3 dB) was significantly higher than in apical myocardium (13.2 +/- 0.6 dB, p less than 0.05). There was no significant difference in the cyclic variation in relative backscatter among thrombus, ischemic myocardium, or intracavitary blood. Thus, the quantitative assessment of the acoustic properties of left ventricular thrombi can be useful in their detection and in the differentiation from myocardium and intracavitary signals.     

Reversal of left ventricular intracavitary gradient with intracavitary diastolic regurgitation in hypertrophic obstructive cardiomyopathy

A 73 year old man presented with angina and nonsustained ventricular tachycardia. Cardiac catheterization revealed the dynamic systolic intracavitary gradient of hypertrophic obstructive cardiomyopathy. Abnormal isovolumetric relaxation resulted in the development of a diastolic gradient from the left ventricular outflow tract to the left ventricular apex accompanied by intracavitary regurgitation of contrast material from the outflow tract to the left ventricular body during left ventriculography. This case provides hemodynamic and angiographic confirmation of abnormal isovolumetric relaxation in this syndrome and insight into its mechanism.     

Radiofrequency Catheter Ablation of Idiopathic Left Ventricular Tachycardia:

Idiopathic Left Ventricular Tachycardia. Introduction: Idiopathic left ventricular tachycardia with a QRS pattern of right bundle branch block and left-axis deviation constitutes a rare but electrophysiologically distinct arrhythmia entity. The underlying mechanism of this tachycardia, however, is still a matter of controversy. This report describes findings in a 42-year-old man who underwent successful radiofrequency catheter ablation of idiopathic left ventricular tachycardia.
Methods and Results: On electrophysiologic study, the tachycardia was reproducibly induced and terminated with double ventricular extrastimuli. Intravenous verapamil terminated the tachycardia whereas adenosine did not. Detailed left ventricular catheter mapping during sinus rhythm revealed a fragmented delayed potential at the mid-apical region of the inferior site near the posterior fascicle of the left bundle branch. At the same site, continuous electrical activity throughout the entire cardiac cycle was recorded during ventricular tachycardia. Repeated spontaneous termination of this continuous electrical activity in late diastole was followed immediately by termination of the tachycardia. Single application of radiofrequency current for 20 seconds at this site completely abolished inducibility of the tachycardia. After catheter ablation, at the identical site of preablation recording of the fractionated potential during sinus rhythm, no fragmented delayed activity could be recorded. There was no complication from the ablation procedure.
Conclusion: The preablation recordings of fragmented delayed potentials during sinus rhythm and continuous diastolic electrical activity during tachycardia, together with ablation characteristics and previously reported electrophysiologic properties of this arrhythmia, may further support microreentry as the underlying mechanism in idiopathic left ventricular tachycardia.     

Effect of excision of ventricular myocardium on delayed potentials detected by the signal-averaged electrocardiogram in patients with ventricular tachycardia

The ability of surgical excision of electrically abnormal ventricular myocardium to either abolish delayed potentials or modify their timing was investigated in 21 patients with spontaneous ventricular tachycardia (VT) late after myocardial infarction. This study also examined whether modification of delayed potentials after surgery was associated with loss of ability to induce VT or improvement in left ventricular function. Signal averaging of the electrocardiogram (ECG), programmed stimulation and radionuclide ventriculography were performed preoperatively and were repeated 10 to 14 days postoperatively. At preoperative investigation, all patients had delayed potentials on the signal-averaged ECG and inducible VT at programmed stimulation. In 7 patients (33%), delayed potentials were abolished by surgery, exceeding the baseline variability of 8.5% for detection of delayed potentials. VT was no longer inducible postoperatively in 16 patients (76%), including the 7 in whom delayed potentials were no longer detectable. In the patients in whom VT was no longer inducible, mean ventricular activation time decreased from 178 ms preoperatively to 151 ms postoperatively (standard error of the mean difference = 6 ms, p less than 0.001). In the 5 patients with inducible VT postoperatively, no significant change in mean ventricular activation time was seen, 181 vs 171 ms (standard error of mean difference = 9 ms). Reductions in ventricular activation time were not associated with an improvement in left ventricular ejection fraction unless aneurysmectomy was performed in addition to excision of electrically abnormal myocardium. Thus, the signal-averaged ECG may have a role in assessing the efficacy of antiarrhythmic surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metastatic ocular melanoma to the left ventricle inducing near-syncope attacks in an 84-year-old woman

Cardiac tumors may represent mechanical causes for syncope by limiting left ventricular filling and/or by obstructing the left ventricular outflow tract. Malignant melanoma is known to metastasize to the myocardium or pericardium, but there are only a very limited number of reports describing endocardial involvement by the tumor. We describe herein an 84-year-old woman who presented with daily near-syncope episodes, 9 years after treatment for a choroidal melanoma. The echocardiography and the pathologic examination revealed a metastatic melanoma. This is the first reported case of an ocular melanoma metastasizing to the heart and presenting as a left ventricular intracavitary pedunculated mass.     

Peripheral emboli from left ventricular thrombi of different echocardiographic appearance in acute myocardial infarction

In four patients with anterior wall acute myocardial infarction (AMI) and left ventricular thrombi diagnosed by two-dimensional (2-D) echocardiography, disappearance of left ventricular thrombi was demonstrated by 2-D echocardiography immediately after the patients had suffered peripheral emboli. Two thrombi were pendulous with free motion during the cardiac contractions; one of these consisted of two separated pendulous clots that disappeared after two episodes of embolization six and 16 days, respectively, after the onset of AMI. Two thrombi were initially broad based, flat, and without intracavitary motion. One thrombus caused two episodes of peripheral emboli; the other began as a flat thrombus without intracavitary motion but progressed to show central echolucency and, then, vigorous intracavitary motion of the margin prior to embolization. Five of six embolic episodes occurred when these patients were receiving high-dose anticoagulants. These anticoagulants were administered once the thrombi were diagnosed. Left ventricular thrombi of very different appearance on 2-D echocardiography may cause embolization, which may occur during therapeutic anticoagulation administered after thrombi have developed in patients with AMI.     

Mega-epsilon waves on 12-lead ECG—just another case of arrhythmogenic right ventricular dysplasia/cardiomyopathy?

Epsilon wave, the post-excitation small squiggles at the beginning of ST segment that first named by Fontaine, is a well-known ECG phenomenon frequently associated with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). Epsilon waves are caused by post excitation of the myocytes in the right ventricle due to myocardial scaring. Increasing evidence suggests that cardiac sarcoidosis might produce the pathological substrate required for production of epsilon waves. Therefore differentiating these two entities is of paramount clinical importance. Here we report a case demonstrating mega-epsilon wave, right ventricular dilatation and inducible ventricular tachycardia (VT) that was initially diagnosed as ARVD/C by the Task Force Criteria. However after a thorough evaluation, diagnosis of cardiac sarcoidosis was confirmed by the evidence of non-caseating granulomas from endomycardial biopsy.     

Arrhythmogenic right ventricular dysplasia: a clinical model for the study of chronic ventricular tachycardia

Arrhythmogenic right ventricular dysplasia (ARVD) is a recently individualised clinical entity which sometimes presents with episodes of ventricular tachycardia (VT). These attacks may be resistant to anti-arrhythmic therapy and new therapeutic approaches have been developed for the treatment of this condition. These new methods are mainly surgical, based on the analysis of the electrical activation of the heart in sinus rhythm and during VT. This approach has increased our understanding of the physiopathology of VT, not only in the context of ARVD, but also in the most commonly encountered clinical setting of VT, after myocardial infarction. Electrophysiological study of the epicardial activation of the dysplastic zones has demonstrated the presence of delayed potentials recorded after the end of the QRS complex. This can be explained by the histopathology of these tissues. ARVD is characterised histologically by partial degeneration of the myocardial wall. Most of the muscle fibers are replaced by fatty tissue in the middle of which some healthy fibers survive. These changes are mainly observed in the intramyocardial and subepicardial layers, the subendocardium being almost normal. Strands of isolated muscle fibers within the non-conducting fatty degeneration may lead to very delayed activation with respect to the adjacent healthy tissues. The propagation of activation is delayed as it passes through this plexiform structure and in the zones adjacent to healthy muscle were reentry phenomena may arise. In ARVD, these changes are mainly located over the right ventricle, so explaining the right ventricular origin of most forms of VT observed in this condition. However, we have also observed a case which suggested an isolated arrhythmogenic left ventricular dysplasia. Epicardial mapping localizes the point of origin of VT in zones situated between the slow and normally conducting tissues. Simple ventriculotomy, a full thickness section of the ventricular wall, at the point of epicardial breakthrough of the VT prevents recurrence in the great majority of patients. The same pathophysiological concepts may be applied to VT complicating myocardial infarction but in this situation the myocardial fibers capable of slowly conducting the activation are isolated within the fibrous tissue in the border zone of the infarct. The point of origin of VT is usually within the interventricular septum with a point of epicardial breakthrough which could be located some distance away. Different surgical techniques have been developed to deal with this condition. Encircling endocardial ventriculotomy isolates the arrhythmogenic zone from the rest of healthy tissues by tracin     

Dynamic intraventricular obstruction during dobutamine stress echocardiography. A new observation.

BACKGROUND. The implications of hypotension occurring during dobutamine stress echocardiography have not been elucidated. We observed in some patients that hyperdynamic left ventricular function developed during dobutamine stress echocardiography and hypothesized that intracavitary obstruction was occurring and might account for hypotension in some patients. METHODS AND RESULTS. Fifty-seven consecutive patients undergoing dobutamine stress echocardiography underwent pulsed-wave and continuous-wave Doppler examination of the left ventricular cavity at rest and at peak dobutamine infusion. The development of an intraventricular gradient with dobutamine stress was defined as a late-peaking left ventricular Doppler velocity profile that exceeded basal velocity by at least 1 m/sec. During dobutamine stress testing, left ventricular outflow velocity or intracavitary velocity increased in all patients. Obstruction occurred in 12 patients (21%, group 1). Group 2 was the remaining 45 patients. Peak velocities in group 1 ranged from 2.0 to 5.0 m/sec (mean, 3.5 m/sec), and the mean increase from velocity at rest was 2.3 m/sec. The mean change in systolic blood pressure was significantly lower in patients in group 1 (-15 versus 4 mm Hg, p = 0.02). When the 18 patients with an ischemic response to stress testing (evidenced by new or worsening wall motion abnormalities) were excluded from analysis, systolic blood pressure response was still significantly different for the two groups (-19 versus 2 mm Hg, p = 0.03). CONCLUSIONS. Dynamic left ventricular obstruction is a new observation; it may develop frequently in patients undergoing dobutamine stress echocardiography. Obstruction rather than ischemia may explain a decrease in blood pressure during dobutamine stress echocardiography.     

Effect of Procainamide, Mexiletine, and Propranolol on Ventricular Activation Time Recorded at Cardiac Mapping in Chronic Canine Myocardial Infarction

Delayed potentials detected during sinus rhythm appear to be markers for ventricular tachyarrhyth mias associated with ch ronic myocardial infarction. This study investigated whether intravenous Class I and Class II antiarrhythmic drugs could affect delayed potentials detected at cardiac mapping in dogs studied 1–2 weeks after anterior myocardial infarction.
Procainamide at therapeutic serum levels (17–34 μmol/L) caused prolongation of delayed potentials (first degree block), the mean change in duration of ventricular activation being + 19.4 ± 5.0 msec (n = 4, p <0.05). At serum levels above the therapeutic range, procainamide caused first degree block in delayed potentials in three of six animals tested (50%), second degree block (Wenckebach, 2:1 or 3:1 block) in another two animals, and third degree block (complete abolition of delayed potentials) in the remaining animal.
Mexiletine at therapeutic serum levels (3.5–9.0 μmol/L, caused no significant change in delayed potential duration (+3.1 ± 5.7 msec, n = 4). At serum levels above the therapeutic range, first degree block occurred in four of five animals tested (80%), there being no change in the fifth animal. After propranolol (0.2 mg/kg), there was no significant change in delayed potential duration (−2.5 ± 2.5 msec, n = 4).
In conclusion: (1) at standard doses, mexiletine and propranolol have no effect on delayed potentials, but procainamide causes first degree block; (2) at serum levels above the therapeutic range, mexiletine typically causes first degree block, while procainamide causes either first degree or high grade block; (3) ventricular tachyarrhythmias may still be inducible after drugs if delayed potentials persist unchanged or with first degree block.     

Abnormal left ventricular intracavitary flow acceleration in patients undergoing aortic valve replacement for aortic stenosis. A marker for high postoperative morbidity and mortality.

BACKGROUND. We examined the clinical and echocardiographic characteristics of patients undergoing aortic valve replacement for aortic stenosis whose continuous wave Doppler studies showed abnormal intracavitary flow acceleration. METHODS AND RESULTS. The clinical and Doppler echocardiographic records of 53 consecutive patients undergoing aortic valve replacement for aortic stenosis were reviewed. Doppler echocardiography was performed at a mean of 6.6 days (range, 0-22 days) after surgery. Thirteen patients (group 1) had a dagger-shaped high-velocity systolic flow signal indicative of abnormal intracavitary flow acceleration on their postoperative Doppler study; group 2 comprised 40 aortic stenosis patients who underwent aortic valve replacement but had no postoperative evidence of abnormal intracavitary flow acceleration. Group 1 postoperative abnormal intracavitary flow velocities ranged from 1.8 to 6.8 m/sec (mean, 4.9 +/- 0.9 m/sec): Resulting dynamic gradients ranged from 10 to 184 mm Hg (mean, 104.6 +/- 32 mm Hg). Compared with group 2, group 1 patients had a distinctive ventricular geometry with more-pronounced hypertrophy, smaller cavities, and higher ejection fraction. Systolic anterior motion of the mitral valve did not accompany abnormal intracavitary flow acceleration in any patient. Six of 13 group 1 patients suffered postoperative hemodynamic compromise characterized by severe hypotension despite adequate pulmonary capillary wedge pressures; group 1 postoperative mortality was significantly greater than that seen in group 2 patients (38% versus 12%, p less than 0.05). CONCLUSIONS. Abnormal intracavitary flow acceleration after aortic valve replacement for severe aortic stenosis is associated with a distinctive ventricular geometry and supernormal systolic function but not systolic anterior motion of the mitral valve. Such flow acceleration appears to be a marker for increased postoperative morbidity and mortality. Preoperative and postoperative Doppler echocardiography may be useful in risk stratification and guiding therapy.     

A potential method of correcting intracavitary left ventricular filling pressures for the effects of positive end-expiratory airway pressure

Based on the observation that positive end-expiratory airway pressure (PEEP) causes comparable increments in intrapericardial and right-sided intracardiac pressures, we hypothesized that intracavitary left ventricular filling pressures measured in the presence of PEEP can be corrected for increased intrathoracic pressure by subtracting the effects of PEEP on intracavitary right ventricular filling pressures. Ventricular function curves (aortic blood flow vs intracavitary left ventricular end-diastolic pressure [LVEDP]) were generated with and without 15 cm of water of PEEP in eight dogs. All curves were shifted to the right by PEEP (i.e., intracavitary LVEDP was higher for any submaximal level of aortic blood flow). However, when pressures measured in the presence of PEEP were "corrected" by subtracting the corresponding increment in intracavitary right ventricular end-diastolic pressure caused by PEEP at each level of ventricular filling, control and corrected PEEP data points appeared to fall on the same curve in five dogs, and differed only slightly in three dogs. Mean control and corrected PEEP curves derived by averaging polynomial regression coefficients for each condition differed significantly from uncorrected PEEP curves (p less than .05), but not from each other. Analogous curves based on mean left atrial pressure were corrected equally well by subtracting the effects of PEEP on mean right atrial pressure. We conclude that the increments in intracavitary right heart filling pressures caused by PEEP can be used to correct intracavitary left heart filling pressures for the effects of PEEP on intrathoracic pressure.     

Rationale for a direct surgical approach to control ventricular arrhythmias: Relation of specific intraoperative techniques to mechanism and location of arrhythmic circuit

Medically intractable ventricular arrhythmias are a common problem with serious consequences. Direct myocardial surgery aimed at ablation or isolation of the arrhythmic circuit, localized by cardiac mapping, offers an alternative treatment that can eradicate the tachycardia. The success of various surgical approaches depends on an accurate assessment of mechanism, concise localization of the arrhythmic circuit by electrophysiologic means and proper selection of the patients most likely to benefit from the procedure. Most forms of ventricular arrhythmias are due to reentry and are typically associated with an abnormal substrate such as infarction, fibrosis or ventricular aneurysm. However, superficially (epicardially) the activation sequence may appear to resemble an abnormal automatic focus tachycardia. Confirmation of the reentrant nature of the tachycardia depends on demonstrating delayed activation in a region close to, or connected to, the site of origin. This frequently requires multiple intramural electrode recordings or endocardial mapping, or both.In the past, the rationale for surgery or for the specific surgical approach has not always been explicit. It was not always clear why a particular surgical approach terminated or failed to terminate the arrhythmia. In some patients the basis of control of the tachycardia could not be explained and the effect was partly accidental. Successful surgical control of ventricular arrhythmias depends on (1) a more precise clarification of mechanism, specifically a more comprehensive definition of the reentrant structure in the individual patient; (2) improved techniques for cardiac mapping, including simultaneous recording of potentials from multiple areas, aimed intramural-endocardial recordings and immediate (computerized) display of the activation map data; and (3) improved surgical techniques based on (1) and accurately guided by (2).     

Intracavitary electrode catheter cardioversion of atrial tachyarrhythmias in the dog

This study examined factors determining efficacy of intracavitary cardioversion of atrial tachyarrhythmias in closed chest, anesthetized dogs with talc pericarditis. Electrode catheters were positioned transvenously with the cathode in the right atrial appendage. In Group 1 dogs (n = 6), three anode sites (superior and inferior venae cavae ostia and mid-right atrium) were tested with graded energy shocks to determine the lowest effective cardioversion energy at each anode position. In Group 2 dogs (n = 9), multiple cardioversion attempts with energy levels of 0.01 to 5.0 J were used to evaluate reproducibility of energy thresholds. In Group 3 dogs (n = 6) without talc-induced pericarditis, atrial pathologic study was done after five intracavitary shocks (0.5 or 5.0 J). In Group 1, cardioversion was achieved with 0.75 J or less with no significant difference in minimal effective cardioversion energies among the three anode positions tested. In Group 2, 98 (26%) of 372 cardioversion attempts were successful. Intra-animal minimal effective cardioversion energies varied widely, and timing of shocks relative to atrial electrograms did not influence efficacy. Complications were infrequent and included delayed sinus rhythm recovery, transient atrioventricular block and ventricular fibrillation. Ventricular fibrillation occurred in 9 (2.4%) of 372 shocks, and was associated with higher delivered energies (6 of 9 with greater than or equal to 1.0 J) and with shocks delivered 116 to 180 ms after onset of the QRS complex. In Group 3, two dogs had no histologic damage, three dogs had multiple small foci of subendocardial necrosis and in one dog these foci coalesced to involve half the atrial wall thickness. Thus, low energy cardioversion of atrial tachyarrhythmias is feasible using intracavitary electrodes. Synchronization of energy delivery to the QRS complex is important to minimize risk of ventricular fibrillation.     

Hypotension and functional left ventricular obstruction during dobutamine stress echocardiography--two case reports

Although hypotension during dobutamine stress echocardiography has been reported, the mechanism of this response is still controversial. In two patients, a 72-year-old woman and 64-year-old man, with exercise-induced ST-T change, continuous-wave Doppler examination of the left ventricular cavity was performed at baseline and peak dobutamine infusion. No echocardiographic abnormalities at rest or angiographic coronary lesions were observed in either patient. The intracavitary pressure gradient at peak dosage of dobutamine for both patients was 121 mm Hg and 100 mm Hg, and was reproducibly confirmed by cardiac catheterization. During dobutamine infusion, echocardiography or left ventriculography revealed that papillary muscle motion was dramatically augmented by dobutamine and mid-left ventricular obstruction was produced at the systolic phase. Although blood pressure response improved following beta-blocker treatment, intracavitary pressure gradient during dobutamine infusion remained the same. A hypotensive response during dobutamine stress echocardiography may be produced by the development of dynamic intraventricular obstruction and a vasodepression reflex. The exercise-induced electrocardiographic changes may have been related to the systolic pressure augmentation in the mid-to-apical left ventricular cavity.     

Endocardial electrograms from the right ventricular outflow tract after induced ventricular fibrillation in patients with Brugada syndrome.

BACKGROUND: The pathogenesis of Brugada syndrome (BS) is reported to be phase 2 reentry resulting from shortening of the action potential duration at the epicardial site of the right ventricular outflow tract (RVOT). However, several reports have shown a high incidence of ventricular late potentials (LPs) and a high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS) among patients with BS. The aim of this study was to investigate the role of slow conduction for the initiation of VF by PVS in these patients. METHODS AND RESULTS: Endocardial mapping of the RVOT was conducted in 17 patients in whom VF was induced by PVS from the RV apex or RVOT; 11 patients had a positive LP. In 10 patients, RV mapping showed that low-amplitude fragmented and delayed potentials (DPs) were recorded at the RVOT below the pulmonary valve (PV) or between the PV and His bundle electrogram recording site. Electrograms recorded after PVS showed a high incidence of fractionated and disorganized DPs that lead to VF. CONCLUSIONS: Slow conduction at the RVOT may contribute to the induction of VF by PVS. However, the role of slow conduction in spontaneous VF remains controversial.     

Left ventricular isovolumic flow sequence during sinus and paced rhythms: new insights from use of high-resolution Doppler and ultrasonic digital particle imaging velocimetry.

OBJECTIVES: We sought to clarify the role of isovolumic intervals during a cardiac cycle by in vivo visualization of left ventricular (LV) intracavitary flow dynamics. BACKGROUND: Asynchronous LV deformation during isovolumic contraction (IVC) and isovolumic relaxation (IVR) might represent a transient feature of myocardial wall mechanics that reverses the direction of blood flow. METHODS: In 10 beating porcine hearts, the changes in LV intracavitary flow were recorded at baseline and after LV epicardial and right atrial pacing with high-resolution Doppler and contrast echocardiography. Two-dimensional vector flow fields were generated offline from B-mode contrast images with particle imaging velocimetry. RESULTS: During IVC, flow from the LV apex accelerated toward the base, whereas blood from the base was redirected toward the outflow through formation of an anterior vortex. Conversely, during IVR, flow was initially directed toward the apex and then briefly reversed toward the base. Epicardial pacing from the LV base altered the stages of flow redirection during the pre-ejection period and delayed mitral valve closure (28 +/- 14 ms vs. 61 +/- 13 ms, p < 0.001) and aortic valve opening (77 +/- 18 ms vs. 111 +/- 18 ms, p = 0.004). CONCLUSIONS: Isovolumic intervals are not periods of hemodynamic stasis but, rather, phases with dynamic changes in intracavitary flow. Experimentally induced aberrant epicardial electrical activation alters stages of flow redirection and prolongs the pre-ejection period. Normal electromechanical activation through the His-Purkinje system in mammalian hearts maintains an inherent synchrony with the sequence of intracavitary flow redirection.     

Long QT Interval and Ventricular Tachycardia of “Torsade de Pointe” Type in Hypothyroidism

ABSTRACT We have observed two patients with long QT interval, ventricular tachycardias of “torsade de pointe” type and repeated ventricular fibrillation episodes, who also turned out to have significant hypothyroidism. This was suspected from the clinical picture in one patient and after haematological test in the other. In addition to hypothyroidism, both patients had associated factors which may have contributed to the development of the arrhythmia. After having reached an euthyroid state, both patients normalized their QT intervals, were relieved from earlier symptoms of cardiac arrhythmias and exhibited no longer any documented arrhythmia. Before thyroid substitution, both patients had marked signs of delayed ventricular repolarization even by invasive electrophysiological methods. Our observations indicate that hypothyroidism should be considered a possible primary cause in cases with long QT syndrome (LQTS). Furthermore, the possibility of LQTS in patients with hypothyroidism should be considered.