"The artichoke heart": the inverse counterpart of left ventricular apical ballooning.
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Adult↗
Biomedical subjects
Frank Bode
Publications and source records attributed to Frank Bode.
Modulation of ventricular repolarization in patients with transient left ventricular apical ballooning: a case control study.
OBJECTIVE: Even though diffuse T wave inversion and prolongation of the QT interval in the surface electrocardiogram (ECG) have been consistently reported in patients with transient stress-induced left ventricular apical ballooning (AB), ventricular repolarization has not yet been systematically investigated in this clinical entity. BACKGROUND: AB, an emerging syndrome that mimics acute ST-segment elevation myocardial infarction (MI), is characterized by reversible left ventricular wall motion abnormalities in the absence of obstructive coronary heart disease and significant QT interval prolongation. METHODS: We prospectively enrolled 22 consecutive patients (21 women, median age 65 years) with transient left ventricular AB. A total of 22 age-, gender-, body-mass-index-, and left-ventricular-function-matched patients with acute anterior ST-segment elevation MI undergoing successful direct percutaneous coronary intervention for a proximal occlusion of the LAD, as well as 22 healthy volunteers served as control groups. Beat-to-beat QT interval and QT interval dynamicity were determined from 24-hour Holter ECGs, recorded on the third day after hospital admission. RESULTS: There were no significant differences in baseline clinical characteristics, except higher peak enzyme release in MI patients. Compared with MI patients, AB patients exhibited significantly prolonged mean QT intervals and rate-corrected QT intervals (QT: 418 +/- 37 vs 384 +/- 33 msec, P < 0.01; QTcBazett: 446 +/- 40 vs 424 +/- 35 msec, P < 0.05; QTcFridericia: 437 +/- 35 vs 412 +/- 31 msec, P < 0.05). Mean RR intervals tended to be higher in AB patients, without reaching statistical significance (877 +/- 96 vs 831 +/- 102 msec, P = NS). The linear regression slope of QT intervals plotted against RR intervals was significantly flatter in AB patients at both day- and nighttime (QT/RR slopeday: 0.18 +/- 0.04 vs 0.22 +/- 0.06, P < 0.01; QT/RR slopenight: 0.12 +/- 0.03 vs 0.17 +/- 0.05, P < 0.01). CONCLUSION: The present study is the first to demonstrate significant differences of QT interval modulation in patients with transient left ventricular AB and acute ST-segment elevation MI. Even though transient AB is associated with a significant QT interval prolongation, rate adaptation of ventricular repolarization (i.e., QT dynamicity) is not significantly altered, suggesting a differential effect of autonomic nervous activity on the ventricular myocardium in transient AB and in acute MI.
Aged↗
Inadequate ICD discharges due to diaphragmatic electromyopotential oversensing as the first sign of right ventricular lead perforation.
Right ventricular lead perforation, when acute, is a rare but potentially life-threatening complication of implantable cardioverter defibrillator (ICD) therapy. We report about a patient with early lead perforation presenting with repetitive ICD discharges due to oversensing of diaphragmatic electromyopotentials and describe the management of this complication.
Action Potentials↗
Ventricular fibrillation induced by stretch pulse: implications for sudden death due to commotio cordis.
INTRODUCTION: Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity. METHODS: We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. RESULTS: Sudden balloon inflation induced VF when pressure pulses of 208-289 mmHg were applied within a window of 35-88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 +/- 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 +/- 3% to 26 +/- 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation. CONCLUSIONS: Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis.
Action Potentials↗
Cardiac autonomic activity in patients with transient left ventricular apical ballooning.
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Autonomic Nervous System↗
Carvedilol versus metoprolol in patients undergoing direct percutaneous coronary interventions for myocardial infarction: effects on QT dynamicity.
Beta-adrenergic blockers exert significant antiarrhythmic activity during ischemia and reperfusion. To further explore the beneficial effects conferred by alpha-1-adrenoceptor blockade on ventricular repolarization dynamicity in the acute phase of myocardial infarction (AMI), we compared carvedilol with metoprolol in the setting of primary percutaneous coronary intervention (PCI). In a prospective study, 100 consecutive patients undergoing primary PCI for AMI were randomized to metoprolol 200 mg/day versus carvedilol 25 mg/day. The first oral dose of study drug was administered and a 24-hour ambulatory electrocardiogram recorded upon hospital admission. Slopes of the linear QT/RR regression were determined before and after reperfusion. A total of 38 recordings of patients treated with metoprolol and 34 recordings of patients with carvedilol were eligible for analysis of QT/RR slopes. The two study groups were similar with respect to age, gender, TIMI perfusion grades, ventricular function, duration of ischemia, and site and size of infarction. Mean RR- and QT-intervals were similar to the metoprolol and carvedilol groups, before and after PCI. Likewise, there was no significant difference in QT/RR slopes between the metoprolol and carvedilol groups before PCI. In contrast, after PCI, there was a trend toward lower QT/RR slopes in the metoprolol group (from 0.18 +/- 0.07 to 0.17 +/- 0.08), and a significant decrease in QT/RR slopes in the carvedilol group (from 0.17 +/- 0.07 to 0.14 +/- 0.09). In patients undergoing successful direct PCI for AMI, treatment with carvedilol, in contrast to metoprolol, was associated with a significant decrease in QT-RR slopes, suggesting greater cardiac electrical stability.
Adrenergic alpha-Antagonists↗
Carvedilol versus metoprolol in the acute phase of myocardial infarction:.
Beta-adrenergic blockers provide significant cardioprotection during acute ischemia and reperfusion. To further explore the effects of additional alpha-1-adrenoceptor blockade on autonomic modulation in acute myocardial infarction (AMI), carvedilol was compared with metoprolol in the setting of primary percutaneous coronary interventions (PCI). In a prospective study, 100 consecutive patients (61.1 +/- 11 years; 23 females) undergoing primary PCI for AMI were randomly assigned to metoprolol 200 mg/day vs carvedilol 25 mg/day. The first oral dose of study drug was administered upon hospital admission, and a 24-hour ambulatory electrocardiogram was recorded. A total of 40 recordings of patients assigned to metoprolol and 39 of patients assigned to carvedilol were eligible for analysis of heart rate turbulence. Turbulence onset (TO), turbulence slope (TS), and turbulence timing were measured after ventricular premature beats (VPBs). The mean value of the 10 preceding RR intervals (mean RR) before VPBs was also measured. There were no significant differences in mean age, gender distributions, TIMI perfusion grades, left ventricular ejection fraction, site and size of infarction, duration of ischemia, and mean 24-hour heart rate between the two groups. Though the mean RR were not significantly different (metoprolol 863.1 +/- 157 ms; carvedilol 839.6 +/- 151 ms), there was a trend toward lower values of TO in the carvedilol group (-0.015 +/- 0.016 vs -0.012 +/- 0.023%; P = NS) and significantly higher values for TS in the metoprolol group (6.96 +/- 5.8 vs 5.6 +/- 4.22; P < 0.05). Turbulence timing was similar in both groups (metoprolol 5.8 +/- 2.4 vs carvedilol 6.1 +/- 2.1). In patients undergoing direct PCI for AMI, treatment with carvedilol, in contrast to metoprolol, was associated with a higher early acceleration and a lower deceleration of heart rate after VPBs, indicating differing effects on baroreceptor response due to additional alpha-1-adrenoceptor blockade. These data offer new insights into effects of a broader antiadrenergic therapy on autonomic reflexes in the acute phase of AMI.
Adrenergic beta-Antagonists↗
Changes in heart rate, heart rate variability, and heart rate turbulence during evolving reperfused myocardial infarction.
Depressed cardiac parasympathetic activity is associated with electrical instability and adverse outcomes after myocardial infarction (MI). Heart rate turbulence (HRT), reflecting reflex vagal activity, and heart rate variability (HRV), reflecting tonic autonomic variations are both reduced in the subacute phase of MI. However, the evolution of these components of cardiac autonomic control between subacute and chronic phase of MI has not been defined. We prospectively studied 100 consecutive patients with a recent first MI with ST-segment elevation, who underwent successful direct percutaneous coronary interventions. Beta-adrenergic blockers and angiotensin-converting enzyme (ACE) inhibitors were administered according to the state-of-the-art medical practice guidelines. HRT and HRV were measured from 24-hour ambulatory electrocardiographic recordings 10 days and 12 months after the index MI. There was no significant difference in mean RR interval between the subacute and chronic phase of MI (875 +/- 145 versus 859 +/- 122 ms). Indices of HRV increased significantly during the observation period (SDNN: from 88.8 +/- 26.8 to 116.0 +/- 35.7 ms, P < 0.001; SDNNi: from 37.9 +/- 15.9 to 46.0 +/- 16.3 ms, P < 0.001; SDANN: from 79.6 +/- 34.7 to 105.6 +/- 35.4 ms, P < 0.001). In contrast, there were no significant changes in indices of HRT (turbulence onset: from -0.008 +/- 0.022 to -0.012 +/- 0.025%; turbulence slope: from 7.78 +/- 5.9 to 8.06 +/- 6.8 ms/beat). In contrast to reflex autonomic activity, there was a significant recovery of tonic autonomic activity within 12 months after MI. These different patterns of recovery of reflex versus tonic cardiac autonomic control after MI need to be considered when risk stratifying post-MI patients.
Aged↗
Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention.
BACKGROUND: In the thrombolytic era, the occurrence of accelerated idioventricular rhythm (AIR) has been proposed to be a specific marker for successful reperfusion. The incidence, prognostic implications, and potential modulating mechanisms of AIR after successful restoration of antegrade flow by means of modern reperfusion therapy (i.e., direct percutaneous coronary intervention (PCI)) has thus far not been investigated. METHODS: We prospectively investigated 125 consecutive patients undergoing direct PCI for a first acute myocardial infarction (AMI). The incidence of AIR was determined from 24-hour Holter monitoring, initiated prior to PCI. RESULTS: AIR appeared in 19 patients (15.2%). There were no significant differences between patients with or without AIR regarding baseline clinical characteristics. The incidence of AIR was not different between patients with TIMI 2 and 3 flow (13% vs 16%). There were no differences in the incidence of major cardiac events within 12-month follow-up in patients with and without AIR. Patients with AIR exhibited higher mean R-R intervals (mean 24-hour R-R interval: 871.3 +/- 121 vs 796.4 +/- 100 ms, P < 0.01), higher hourly mean values of heart rate variability (SDNN, 64.7 +/- 26 vs 49.4 +/- 20 ms, P < 0.01; rMSSD, 29.3 +/- 15 vs 22.0 +/- 12 ms, P < 0.01) and lower serum norepinephrine concentrations (60 minute after PCI, 478.9 +/- 357 vs 649.0 +/- 499 pg/ml, P < 0.05). CONCLUSIONS: Our findings indicate that AIR is an nonspecific marker for reperfusion of the infarct-related artery in AMI and thus, predate previous observations of the thrombolytic era. Even though, AIR was associated with higher tonic vagal tone and lower sympathetic activity, the occurrence of AIR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion.
Angioplasty, Balloon, Coronary↗
Left ventricular malposition of pacemaker lead in Chagas' disease.
A 52-year-old Argentinian woman presented with third-degree AV block due to seropositive chronic stage of Chagas' disease. Subsequently, a DDD pacemaker was implanted. Interestingly, a postoperative chest X ray suggested left ventricular lead misplacement, an ECG showed a paced RBBB. Echocardiography confirmed suspected lead malposition in the left ventricle with perforation of a large aneurysm of the interatrial septum that might be related to Chagas' disease. The ventricular lead was successfully repositioned in the right ventricle. Therefore, to avoid lead malposition in Chagas' disease structural cardiac defects should always be ruled out before operation. If a paced RBBB indicates malposition, different fluoroscopic projections should be used to verify lead position.
Bundle-Branch Block↗
Pocket hematoma after pacemaker or implantable cardioverter defibrillator surgery: influence of patient morbidity, operation strategy, and perioperative antiplatelet/anticoagulation therapy.
STUDY OBJECTIVES: Pocket hematoma is a common complication after pacemaker or implantable cardioverter defibrillator (ICD) implantation. Thus, we investigated the influence of patient comorbidity, implantation strategy, operator experience, antiplatelet therapy, and anticoagulation therapy on hematoma rate. DESIGN: Between 1990 and 2002, a total of 3,164 devices (pectoral pacemakers, 2,792; ICDs, 372) were implanted at our institution. Predictors of hematoma occurrence were determined prospectively and were analyzed by multivariate regression analysis. Operator experience was graded by individual implantation number, as follows: low, < 50; medium, 50 to 100; and high, > 100. RESULTS: The incidence of pocket hematoma was 4.9%, leading to prolonged hospitalization in 2.0% of all patients. Reoperation for pocket hematoma was required in 1.0% of patients. High-dose heparinization (hazard ratio [HR], 4.2), combined acetylsalicylic acid (ASA)/thienopyridine treatment after coronary stenting (HR, 5.2), and low operator experience (HR, 1.6) were independently predictive of hematoma development. Therapy with ASA alone did not increase the hematoma rate compared to patients who did receive antiplatelet or anticoagulation therapy (3.1% vs 2.5%, respectively; difference not significant). In patients with nonvalvular atrial fibrillation, postoperative high-dose heparinization substantially increased the hematoma rate (10.7% vs 2.9%, respectively; p < 0.001) without reducing the rate of arterial embolism within the first month after implantation (0.18% vs 0.21%, respectively; difference not significant). The infection rate (0.28% within 3 months after implantation) was not influenced by the presence of the pocket hematoma. CONCLUSIONS: The use of high-dose heparinization and combined ASA/thienopyridine treatment are highly predictive for the occurrence of intraoperative bleeding and pocket hematoma in patients who have undergone pacemaker and ICD surgery. We propose recommendations for the management of antiplatelet and anticoagulation therapy in patients undergoing these interventions.
Aged↗
Impact of infarct-related artery flow on QT dynamicity in patients undergoing direct percutaneous coronary intervention for acute myocardial infarction.
BACKGROUND: Complete coronary artery reperfusion in acute myocardial infarction (AMI) has been shown to significantly improve survival. Electrical stability may be the decisive mechanism for this beneficial effect. Because electrical stability is largely dependent on ventricular repolarization, we sought to determine the impact of a modern reperfusion strategy (ie, direct percutaneous coronary intervention [PCI]) on QT dynamicity in AMI and examined its association with infarct-related artery flow. METHODS AND RESULTS: We prospectively investigated QT dynamicity in 128 patients undergoing direct PCI for a first AMI. Slopes and correlation coefficients of the linear QT/RR regression were determined in the time interval before reperfusion, within the initial hour after reperfusion, and within the remaining recording period from Holter ECG recordings, which were initiated on admission. Subgroup analysis based on TIMI 3 (n=100) and TIMI 2 (n=28) flow after PCI revealed no significant differences in QT/RR slope before PCI (0.145+/-0.12 versus 0.160+/-0.19,P=NS). After PCI, QT/RR slopes increased only in the TIMI 2 subgroup (P<0.05). In TIMI 2 patients, QT/RR slopes were significantly steeper in the hour after PCI and in the remaining recording period, respectively (0.155+/-0.12 versus 0.192+/-0.15,P<0.05, and 0.159+/-0.10 versus 0.210+/-0.17,P<0.01). CONCLUSIONS: Alterations of QT dynamicity in patients with incomplete reperfusion may suggest an altered electrical restitution, potentially providing a substrate for serious ventricular arrhythmias. Thus, our findings offer new insights into mechanisms by which complete reperfusion may affect electrical stability.
Angioplasty, Balloon, Coronary↗
Reflex cardiac activity in ischemia and reperfusion: heart rate turbulence in patients undergoing direct percutaneous coronary intervention for acute myocardial infarction.
BACKGROUND: Abnormal heart rate turbulence (HRT) is associated with an increased risk of mortality in the chronic phase of myocardial infarction (MI) in the prethrombolytic and thrombolytic eras. However, the impact of direct percutaneous coronary intervention (PCI) on HRT in the acute phase of MI and its association to the epicardial infarct-related arterial flow has not been examined. METHODS AND RESULTS: We investigated HRT in 126 patients undergoing direct PCI for a first MI. Turbulence onset and turbulence slope were determined before reperfusion, during the initial 2 hours after reperfusion, and during hours 6 to 24 after reperfusion. HRT significantly improved after PCI. There were no significant differences in baseline clinical characteristics between Thrombolysis in Myocardial Infarction Trial classification (TIMI) 2 (n=28) and TIMI 3 (n=98) flow. After PCI, turbulence slope increased (13.2+/-11 to 18.1+/-12 ms/beat, P<0.001) and turbulence onset decreased (-0.008+/-0.04% to -0.023+/-0.04%, P<0.01) in patients with TIMI 3 flow after PCI, whereas there were no significant alterations of turbulence slope (12.2+/-10 to 12.8+/-6.5 ms/beat) and turbulence onset (-0.009+/-0.05% to -0.003+/-0.03%) in patients with TIMI 2 flow. CONCLUSIONS: The improvement of HRT after successful reperfusion is a previously unreported effect of direct PCI for acute MI, reflecting rapid restoration of baroreceptor response. The persistent impairment of HRT after PCI in patients with TIMI 2 flow indicates a sustained blunted baroreflex response and may reflect a more severe microvascular dysfunction.
Angioplasty, Balloon, Coronary↗
Long-term complication rates in ventricular, single lead VDD, and dual chamber pacing.
A higher incidence of pacemaker related complications has been reported in DDD systems as compared to VVI devices. The implantation of single lead VDD pacemakers might reduce the complication rate of physiological pacing in patients with AV block. In a retrospective study, the data records of 1,214 consecutive patients with pacemaker implantation for AV block between 1990 and 2001 (VVI 36.5%, DDD 32.9%, VDD 30.6%) were analyzed. Complications requiring surgical interventions were compared during a follow-up period of 64 +/- 31 months. Operation and fluoroscopic times were longer in DDD pacemaker implantation compared to VDD and VVI devices:58 +/- 23 versus 39 +/- 10 and 37 +/- 13 minutes (P<0.001), 9.2 +/- 5.2 versus 4.1 +/- 2.4 and 3.5 +/- 2.3 minutes, respectively. Differences remained significant after correction for covariates. In a multivariate Cox regression model, the corrected complication hazard of a DDD pacemaker implantation was increased by 3.9 (1.4-11.3) compared to VVI and increased by 2.3 (1.1-4.5) compared to VDD pacing. Higher complication rates in DDD pacing were mainly due to a higher incidence of early reoperation for atrial lead dysfunction, whereas the long-term complication rate was not different from VDD or VVI pacing. Early and long-term complication rates did not differ between VDD and VVI pacemaker systems. In conclusion, operation time and complication rates of physiological pacing are reduced by VDD pacemaker implantation achieving values comparable to VVI pacing. Thus, single lead VDD pacing can be recommended for patients with AV block.
Adolescent↗
R wave undersensing caused by an algorithm intended to enhance sensing specificity in an implantable cardioverter defibrillator.
This article reports on a case of ventricular undersensing despite normal R wave amplitudes during sinus rhythm in an ICD patient. Undersensing of ventricular signals was noted without any evidence of lead dislocation or variation in signal amplitude. Undersensing was due to an exceptionally small R wave signal width and a feature of the Biotronik sensing algorithm designed to avoid oversensing. This algorithm, intended to enhance the sensing specificity of the device, requires registration of two consecutive points above the maximum programmed sensitivity for a ventricular sense event. After modifying the algorithm to a single point registration undersensing disappeared.
Aged↗
Temporal repolarization inhomogeneity and reperfusion arrhythmias in patients undergoing successful primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction: impact of admission troponin T.
BACKGROUND: The presence of admission cardiac troponin-T (cTnT) is a means of identifying a high-risk subgroup in patients with acute ST-segment elevation myocardial infarction (AMI). Because a substantial number of these patients has malignant ventricular arrhythmias, we hypothesized that there is a relation between cTnT status on admission and inhomogeneity of ventricular repolarization, and we tested this assumption in the setting of primary percutaneous coronary intervention (PCI). METHODS: Temporal fluctuations of ventricular repolarization were studied during and after primary PCI (Thrombolysis In Myocardial Infarction [TIMI] 2 and 3) in 94 consecutive patients with a first AMI by continuous beat-to-beat QT-interval measurement, performed with Holter monitoring initiated on admission. Troponin-T levels on admission were >0.1 ng/mL in 53 patients (cTnT+) and <0.1 ng/mL in 41 patients (cTnT-). There were no significant differences in baseline clinical characteristics between the groups. RESULTS: The incidence of severe reperfusion arrhythmias (RAs) was significantly higher in patients in the cTnT+ group within the first 2 hours after recanalization. The course of the QT interval revealed a significant decline (P <.001) after recanalization of the infarcted vessel within 10 hours in both groups; however, hourly values were significantly lower and normalization of the QT parameters was more rapid in patients in the cTnT- group than patients in the cTnT+ in this period (QTc, 438.5 +/- 28.3 ms vs 449.3 +/- 35.3 ms [hour 1, P <.01]; 413.6 +/- 35.8 ms vs 420.1 +/- 39.2 ms [hour 10, P <.05]). QT-interval variability also significantly declined within 4 hours after PCI (P <.001), and likewise, patients in the cTnT- group exhibited lower values in this period (QTSD, 29.7 +/- 6.8 ms vs 33.5 +/- 10.5 ms [hour 1, P <.01]; 23.0 +/- 6.1 ms vs 25.9 +/- 7.5 ms [hour 4, P <.01]). CONCLUSIONS: Positivity of cTnT on admission is associated with a significantly higher temporal inhomogeneity of ventricular repolarization and a higher incidence of malignant RAs, which suggests more advanced microvascular injury. Early successful primary PCI ultimately results in a significant recovery of parameters of QT interval and mean RR interval in all patients, although it was significantly delayed in patients in the cTnT+ group.
Angioplasty, Balloon, Coronary↗
Alternans of atrial action potentials during atrial flutter as a precursor to atrial fibrillation.
BACKGROUND: The mechanisms underlying the transition of typical atrial flutter (Afl) to fibrillation (AF) remain unclear. We set out to test the hypothesis that Afl disorganizes to AF via alternans of atrial action potentials. METHODS AND RESULTS: In 38 patients with Afl, monophasic action potentials (MAPs) were recorded at the isthmus and either high or low right atrium (HRA, LRA) during overdrive pacing to 160 ms or to the initiation of AF, whichever came first. MAP duration measured at 90% repolarization was longer at the isthmus in all patients, and failed to shorten with rate, compared with the HRA (n=38) or LRA (n=5). In 20 patients who developed AF, progressive pacing first caused alternans of isthmus MAP duration and amplitude at mean cycle length of 219+/-45 ms, followed by AF at a mean onset cycle length of 184+/-38 ms. Subsets of this group showed spontaneous action potential duration alternans at the isthmus (11 of 20 patients) and 2:1 isthmus conduction block immediately preceding AF (4 of 20 patients). In the 18 patients who did not develop AF, MAP alternans was less common (9 of 18 patients; P<0.0003), and occurred only at faster pacing (cycle length=169+/-25 ms; P<0.05). CONCLUSIONS: In patients with typical Afl, action potential duration rate maladaptation at the isthmus may lead to action potential duration alternans and conduction block preceding the transition to AF. These isthmus characteristics may enable the spontaneous initiation of AF through wavefront fractionation and may explain the benefits of isthmus ablation in preventing AF recurrence.
Action Potentials↗
Upstream stimulation versus downstream stimulation: arrhythmogenesis based on repolarization dispersion in the human heart.
OBJECTIVE: The purpose of this study was to test the hypothesis that a ventricular tachycardia (VT) induction site has a shorter action potential duration (APD) and effective refractory period (ERP) than a noninducing site, resulting in collision against longer ERP ("upstream") as opposed to shorter ERP ("downstream," no collision). BACKGROUND: Induction of sustained VT is often feasible at one stimulation site while application of an identical pacing protocol to another site fails to provoke VT. METHODS: Sixty-nine patients undergoing programmed stimulation for VT inducibility had monophasic action potential recording/pacing catheters placed in the right ventricular outflow tract (RVOT) and right ventricular apex (RVA) simultaneously. Up to three extra-stimuli were introduced in 5 to 10 ms decrements until ERP was reached. Upon completion of a drive cycle at one stimulation site, it was repeated at the other. RESULTS: Thirty-eight patients had inducible VT, nine exclusively by RVA pacing and nine exclusively by RVOT pacing. Action potential duration and ERP at the induction site were significantly shorter (12 +/- 15 ms, p <0.05 and 22 +/- 14 ms, p < 0.01, respectively, at 600 ms basic cycle length) than at the noninduction site. Dispersion of repolarization between corresponding APD at the two sites was 58 +/- 41 ms during baseline stimulation (S1) at the inducing site but only 37 +/- 23 ms at the noninducing site (p < 0.05). Dispersion increased during extra-stimulus application (p < 0.05), reaching a maximum of 75 +/- 45 ms during VT induction, but only 53 +/- 33 ms during extra-stimulation at the noninduction site. CONCLUSIONS: Site specificity of VT induction underscores the role of dispersion of repolarization and refractoriness in facilitating re-entry arrhythmias. Upstream stimulation at a site with short repolarization produces larger dispersion and facilitates VT induction.
Action Potentials↗