62 research outputs found
Typical Atrial Flutter Ablation: Demonstration of Cavo-Tricuspid Isthmus Block Aided by a Halo Catheter
A 61-year-old gentleman with one-year history of atrial flutter (see typical saw-tooth appearance of flutter –F waves in the inferior ECG leads in Panel A) refractory to antiarrhythmic agents was submitted to cavotricuspid isthmus ablation. During the procedure, use of an eicosapolar halo catheter (Panel B, arrow) helped to demonstrate the counterclockwise direction of activation (from proximal pole pairs Halo 10 toward Halo 1, Panel D). Upon completion of the ablation line along the isthmus, conversion of atrial flutter into sinus rhythm was noted (Panel C, arrow). With the aid of the halo catheter, bidirectional block could be easily determined by pacing near the coronary sinus os (Panel E, arrow) and recording the late activation of Halo 1, which was withdrawn to the lateral wall of the low right atrium, and finally pacing at the low lateral wall (Panel F, arrow) and recording late activation by the catheter near the coronary sinus os... (excerpt
Pathophysiology of Resistant Hypertension: The Role of Sympathetic Nervous System
Resistant hypertension (RH) is a powerful risk factor for cardiovascular morbidity and mortality. Among the characteristics of patients with RH, obesity, obstructive sleep apnea, and aldosterone excess are covering a great area of the mosaic of RH phenotype. Increased sympathetic nervous system (SNS) activity is present in all these underlying conditions, supporting its crucial role in the pathophysiology of antihypertensive treatment resistance. Current clinical and experimental knowledge points towards an impact of several factors on SNS activation, namely, insulin resistance, adipokines, endothelial dysfunction, cyclic intermittent hypoxaemia, aldosterone effects on central nervous system, chemoreceptors, and baroreceptors dysregulation. The further investigation and understanding of the mechanisms leading to SNS activation could reveal novel therapeutic targets and expand our treatment options in the challenging management of RH
Ablation Techniques in a Patient with a Right Accessory Pulmonary Vein. Is it Always Feasible?
A 32-year-old woman with lone paroxysmal atrial fibrillation had two pulmomary vein isolation procedures over 1 year, by means of the circular multipolar duty-cycled radiofrequency PVAC in the first and the Thermocool® SmartTouchTM catheter in the second procedure. Following both procedures, the patient remained highly symptomatic on a weekly to monthly basis and a third procedure by using the second generation of cryoballoon Arctic Front AdvanceTM. Right inferior pulmonary vein was completely reconnected and an extreme hockey stick configuration was necessary in order to achieve complete occlusion and isolation. Thirty months later the patient remains symptom free in the absence of any therapy
Ablation Techniques in a Patient with a Right Accessory Pulmonary Vein. Is it Always Feasible?
A 32-year-old woman with lone paroxysmal atrial fibrillation had two pulmomary vein isolation procedures over 1 year, by means of the circular multipolar duty-cycled radiofrequency PVAC catheter in the first and the Thermocool® SmartTouchTM catheter in the second procedure. Following both procedures, the patient remained highly symptomatic on a weekly to monthly basis and a third procedure was performed by using the second generation of cryoballoon Arctic Front AdvanceTM. Right inferior pulmonary vein was completely reconnected and an extreme hockey stick configuration was necessary in order to achieve complete occlusion and isolation. Thirty months later the patient remains symptom free in the absence of any therapy. Rhythmos 2016;11(4):96-97
Redo Ventricular Tachycardia Ablation in a Frail Patient with Ischemic Cardiomyopathy. Benefit of Survival versus Risk of Complications
We present a case of repeated successful ventricular tachycardia ablation in an elderly frail post-myocardial infarction patient who presented with recurrent and often incessant episodes of slow ventricular tachycardia. An 85-year old thin male was presented with a hemodynamically stable, slow ventricular tachycardia, temporarily terminated after multiple anti-tachycardia pacing attempts. A previous recent ventricular tachycardia ablation procedure due to multiple ICD activations yielded poor result. Identification and elimination of late potentials was accompanied by final non-inducibility and a free from ventricular tachycardia mid-term outcome
Doppler tissue imaging unmasks right ventricular function abnormalities in HIV-infected patients
Background: We sought to investigate right ventricular (RV) function with Doppler tissue
imaging (DTI) in human immunodeficiency virus (HIV)-infected patients receiving highly-active antiretroviral treatment, without any heart-related symptoms.
Methods: We studied 38 asymptomatic HIV patients (aged 44.5 ± 9.2 years, 22 of them men)
and 25 age-matched and sex-matched controls. All subjects underwent conventional and DTI
estimation of left ventricular (LV) systolic and diastolic function, measuring peak systolic and
diastolic myocardial velocities at the mitral annulus (Sm, Em, Am). Two-dimensional (2-D)
echocardiographic study of the right ventricle (RV) was performed from the four-chamber view, and
RV end-diastolic dimensions were measured. DTI recordings from the RV free wall at the tricuspid
annulus were used to determine systolic (SmRV) and diastolic function (EmRV and AmRV).
Results: HIV-infected patients compared to controls exhibited significantly lower peak systolic
velocities at the septal-SmIVS (7.9 ± 1.3 vs 9.1 ± 1.4 cm/s, p = 0.002) and lateral mitral
annulus - SmLAT (9.8 ± 1.7 vs 11.2 ± 1.3 cm/s, p = 0.025); no difference was observed
regarding conventional 2-D examination of LV systolic and diastolic function and DTI-derived Em and Am. No significant difference occurred between HIV patients and controls
regarding RV end-diastolic dimensions and pulmonary artery systolic pressure. However,
SmRV (13.8 ± 1.6 vs 14.9 ± 2.2 cm/s, p = 0.040), EmRV (11.6 ± 3 vs 13.5 ± 2.6 cm/s, p = 0.028)
and AmRV (10.9 ± 2.5 vs 13.8 ± 4 cm/s, p = 0.003) were significantly reduced in HIV
patients as compared to controls.
Conclusions: DTI unmasks subtle and otherwise undetectable abnormalities of the longitudinal
LV systolic function and both RV systolic and diastolic function, in asymptomatic HIV
patients receiving highly-active antiretroviral treatment. (Cardiol J 2010; 17, 6: 587-593
LEFT VENTRICULAR HYPERTROPHY VERSUS ARTERIAL STIFFNESS AS PREDICTORS OF CORONARY ARTERY DISEASE IN ESSENTIAL HYPERTENSION: DATA FROM A GREEK 6-YEAR FOLLOW-UP STUDY
Effect of Transient Myocardial Ischemia on QT Interval Dispersion Among Patients with Unstable Angina
Objective: Our aim was to examine the effect of transient myocardial ischemia on QT interval and QT interval dispersion in patients presenting with unstable angina.Methods: We studied 31 patients (mean age 64±10, 22 men, 16 with an old myocardial infarction, 6 with previous coronary bypass surgery) admitted with unstable angina manifestations. Patients with a history of complex ventricular ectopy, malignant ventricular arrhythmias, advanced congestive heart failure or antiarrhythmic drug therapy were excluded. The uncorrected and corrected QT interval and QT dispersion were measured during angina as well as after the relief of pain.Results: The RR intervals were not significantly changed by the ischemic event (879±121 ms at rest to 877±173 ms during angina). However, both the uncorrected and corrected QT intervals were significantly increased during angina (from 410±45 ms and 440±41 ms at rest to 425±53 ms and 460±42 ms during angina respectively, p<0.05 for both). Similarly, both the uncorrected (QTd) and the corrected (QTcd) QT dispersion values were significantly prolonged during ischemia (QTd: 58±23 ms at rest to 83±33 ms during ischemia, p<0.001, QTcd: 63±26 ms at rest to 95±36 ms during ischemia, p<0.001). The observed increment in the QTd and QTcd provoked by ischemia was not different among the unstable angina patients with and without old myocardial infarction.Conclusion: Transient myocardial ischemia besides an increase in the QT and QTc intervals provokes an increase in both the corrected and uncorrected QT interval dispersion. Under certain circumstances, this may contribute to the genesis of serious reentry ventricular arrhythmias
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