Caudocranial transseptal approach for placement of endocardial left ventricular leads.

Cardiac resynchronization therapy (CRT) is associated with improvement in the quality of life, hospitalization rates, and mortality in patients with left ventricular dysfunction and evidence of the right ventricle-left ventricle (RV-LV) desynchrony. Implant failure rates and patient outcomes have improved with the advent of quadripolar leads, yet alternatives to traditional coronary sinus (CS) LV lead placement is sought for in a subset of advanced heart failure patients with difficult CS anatomy, phrenic nerve stimulation or in nonresponders. Endocardial left ventricular pacing (EnLVP) in chronically anticoagulated patients has been reported as an alternative using different approaches, techniques, and tools with acceptable short and long term adverse events. We present a case of successful EnLVP achieved for CRT using standard techniques and commonly available tools in a patient on chronic direct oral anticoagulation with recurrent heart failure admissions who failed traditional epicardial LV pacing.

The relationship between the P wave and local atrial electrogram in predicting conduction block during catheter ablation of cavo-tricuspid isthmus-dependent atrial flutter.

PURPOSE: The endpoint for radiofrequency catheter ablation (RFA) of cavo-tricuspid isthmus (CTI)-dependent atrial flutter (AFL) is complete conduction block along the CTI. The purpose of this study is to evaluate the utility of the temporal relationship between the P wave and the local atrial electrograms in determining complete CTI block. METHODS: RFA of CTI was performed in 125 patients (age 63 ± 11 years). During pacing from the coronary sinus (CS), the intervals from the peak of the P wave (Ppeak) in lead V1 to the second component of the local atrial electrogram (A2) along the ablation line (Ppeak-A2) and from the end of the P wave (Pend) to A2 (Pend-A2) were investigated before and after complete block in the first 100 patients (training set). In the next 25 patients (validation set), Ppeak-A2 and Pend-A2 intervals were prospectively assessed to determine CTI block. RESULTS: The mean Ppeak-A2 and Pend-A2 immediately before complete block were - 15±24 and - 39±23 ms compared to 49 ± 17 and 21 ± 16 ms after CTI block (P < 0.0001). Ppeak-A2 ≥ 20 ms and Pend-A2 ≥ 0 ms predicted CTI block with 98% sensitivity and 95% specificity and 96% sensitivity and 100% specificity, respectively. In the validation set, the positive and negative predictive values of Ppeak-A2 ≥ 20 ms or Pend-A2 ≥ 0 ms were 100 and 96%, respectively. The diagnostic accuracy was 98%. CONCLUSIONS: During pacing from the CS, the temporal relationship between the P wave in lead V1 and A2 is a simple and reliable indicator of complete block during RFA of CTI-AFL.

Galectin-3 Regulates Atrial Fibrillation Remodeling and Predicts Catheter Ablation Outcomes.

OBJECTIVES: To determine whether Gal-3 mediates sustained atrial fibrillation (AF)-induced atrial structural and electrical remodeling and contributes to AF perpetuation. BACKGROUND: Galectin-3 (Gal-3) mediates extracellular matrix remodeling in heart failure, but its role in AF progression remains unexplored. METHODS: We examined intracardiac blood samples from patients with AF (N=55) to identify potential biomarkers of AF recurrence. In a sheep model of tachypacing-induced AF (N=20), we tested the effects of Gal-3 inhibition during AF progression. RESULTS: In patients, intracardiac serum Gal-3 levels were greater in persistent than paroxysmal AF and independently predicted atrial tachyarrhythmia recurrences after a single ablation procedure. In the sheep model, both Gal-3 and TGF-ß1 were elevated in the atria of persistent AF animals. The Gal-3 inhibitor GM-CT-01 (GMCT) reduced both Gal-3 and TGF-ß1-induced sheep atrial fibroblast migration and proliferation in vitro. GMCT (12 mg/kg twice/week) prevented the increase in serum procollagen type III N-terminal peptide seen during progression to persistent AF, and also mitigated atrial dilatation, myocyte hypertrophy, fibrosis, and the expected increase in dominant frequency of excitation. Atria of GMCT-treated animals had significantly less TGF-ß1-Smad2/3 signaling pathway activation and expression of α-smooth muscle actin and collagen than saline-treated animals. Ex-vivo hearts from GMCT-treated animals had significantly longer action potential durations and fewer rotors and wavebreaks during AF, and myocytes had lower functional expression of inward rectifier K+ channel (Kir2.3) than saline-treated animals. Importantly, GMCT increased the probability of spontaneous AF termination, decreased AF inducibility and reduced overall AF burden. CONCLUSIONS: Inhibiting Gal-3 during AF progression might be useful as an adjuvant treatment to improve outcomes of catheter ablation for persistent AF. Gal-3 inhibition may be a potential new upstream therapy for prevention of AF progression.

Endocardial ablation of postinfarction ventricular tachycardia with nonendocardial exit sites.

BACKGROUND: Most infarct-related ventricular tachycardias (VTs) have an exit site that can be targeted by endocardial ablation. However, some VT reentry circuits have an exit site that is intramural or epicardial. Even these circuits may have an endocardial component that can be endocardially ablated. OBJECTIVE: To assess the prevalence of postinfarction VTs with a nonendocardial exit site that can be successfully eliminated by endocardial ablation. METHODS: Twenty-eight consecutive patients with postinfarction VT (27 men, age 69 ± 8 years, ejection fraction 0.25% ± 0.15%) were referred for VT ablation. A total of 213 VTs were inducible (cycle length 378 ± 100 ms). Pace mapping was performed throughout the scar, and critical sites were identified for 137 VTs (64.5%). Critical sites identified by entrainment mapping and/or pace mapping were divided into exit and nonexit sites depending on the stimulus-QRS/VT cycle length ratio (S-QRS/VT CL ≤ 0.3 vs>0.3). RESULTS: Endocardial exit sites (S-QRS/VTCL ≤ 0.3) were identified for 100 of 137 VTs. Only critical nonexit sites were identified for 37 of 137 (27%) VTs. Nonexit sites were confined to a smaller area within the endocardium (1.81 ± 1.7 cm(2)) and were located within dense scar (0.28 ± 0.24 mV) further away from the border zone (2.05 ± 2.79 cm) than did the VT exit sites. Exit sites had a larger area of matching pace maps (3.86 ± 1.9 cm(2); P<.01) and were at a closer distance to the border zone (0.93 ± 1.06 cm; P<.01). A total of 133 of 137 VTs were ablated. The success rate was similar for VTs in which exit sites were targeted (n = 90 of 100) and VTs in which only nonexit sites were targeted (n = 36 of 37) (P = .83). CONCLUSIONS: In about one-third of postinfarction VTs for which critical sites were identified, the exit site was not endocardial. Critical nonexit sites that are effective for ablation are often within dense scar at a distance from the border zone and can be missed if only the border zone is targeted.

Echocardiographically detected fibrinous sheaths associated with central venous catheters.

Several million catheters are annually placed in the United States and worldwide for a multitude of clinical conditions. Potential delayed complications relating to central venous catheters include infections, thrombosis and fibrin sheath formation. Fibrin sheaths form frequently around central catheters but seldom cause clinical symptoms by themselves that warrant further investigation. It is likely that with the advent of echocardiographic imaging techniques, these "sleeves" get detected more often, which may result in early and correct diagnosis of this potential hazardous condition. Retained fibrin sleeves can cause malfunction of indwelling catheters, can persist after removal of the catheter, and be a nidus for thrombus formation or vegetation with a potential for distal embolization. Future research directed at creating new coatings with cytotoxic or cytostatic agents is warranted to reduce the incidence of fibrin sheath formation and hence prevent potential complications. We report three cases of persistent fibrin sheaths forming at the site of previously inserted tunneled catheters two of which were complicated by thrombus formation and vegetations.

Impact of medical therapy on atheroma volume measured by different cardiovascular imaging modalities.

Atherosclerosis is a systemic disease that affects most vascular beds. The gold standard of atherosclerosis imaging has been invasive intravascular ultrasound (IVUS). Newer noninvasive imaging modalities like B-mode ultrasound, cardiac computed tomography (CT), positron emission tomography (PET), and magnetic resonance imaging (MRI) have been used to assess these vascular territories with high accuracy and reproducibility. These imaging modalities have lately been used for the assessment of the atherosclerotic plaque and the response of its volume to several medical therapies used in the treatment of patients with cardiovascular disease. To study the impact of these medications on atheroma volume progression or regression, imaging modalities have been used on a serial basis providing a unique opportunity to monitor the effect these antiatherosclerotic strategies exert on plaque burden. As a result, studies incorporating serial IVUS imaging, quantitative coronary angiography (QCA), B-mode ultrasound, electron beam computed tomography (EBCT), and dynamic contrast-enhanced magnetic resonance imaging have all been used to evaluate the impact of therapeutic strategies that modify cholesterol and blood pressure on the progression/regression of atherosclerotic plaque. In this review, we intend to summarize the impact of different therapies aimed at halting the progression or even result in regression of atherosclerotic cardiovascular disease evaluated by different imaging modalities.

R-wave amplitude changes measured by electrocardiography during early transmural ischemia.

BACKGROUND: Changes in the amplitude of the R wave (RWA) on the electrocardiogram (ECG) have been described during acute myocardial ischemia and infarction. However, this has not been well studied in a controlled setting. We hypothesized that significant increase in RWA occurs during early transmural myocardial ischemia. METHODS: We prospectively evaluated changes in RWA in 50 patients during brief episodes of transmural ischemia induced by first balloon occlusion (mean, 38 seconds at 6-10 atmospheric pressures) during elective percutaneous coronary intervention. We recorded 12-lead ECGs at 20-second intervals before and during balloon inflation in 16 right coronary arteries, 14 left circumflex arteries, and 20 left anterior descending arteries. R wave amplitude was digitally measured in each of the 12 leads in every ECG using the ECG interval editor (General Electric HC, Menomonee Falls, WI). Intracoronary (IC) ECGs were also recorded in 4 patients. The mean of the RWA in each lead before balloon inflation was compared to the mean RWA during balloon inflation. RESULTS: R wave amplitude significantly increased during balloon inflation from baseline in limb leads I, II, aVL, and all the precordial leads with the exception of lead V(1). The RWA increase did not reach statistical significance in leads III, aVF, and V(1). Mean RWA increase was consistent in all leads except aVR during the brief episodes of ischemia during initial balloon inflation because of the inverse polarity of this lead. The increase in RWA was seen in most patients (mean, 75%) in whom transmural ischemia was induced by first balloon inflation. Besides, the RWA showed an increase from baseline in 3 patients who had IC-lead recordings. CONCLUSION: R wave amplitude increases significantly in precordial leads (V(2)-V(6)) and limb leads (I, II, aVL) of the surface ECG during brief episodes of transmural ischemia. The increase in RWA might be consistent with the expansion of the left ventricular cavity during ischemia and/or alterations in conduction that are intrinsic to the myocardium.

The efficacy and safety of combination glycoprotein IIbIIIa inhibitors and reduced-dose thrombolytic therapy-facilitated percutaneous coronary intervention for ST-elevation myocardial infarction: a meta-analysis of randomized clinical trials.

OBJECTIVE: We reviewed the literature and performed a meta-analysis comparing the safety and efficacy of adjunctive use of reduced-dose thrombolytics and glycoprotein (Gp) IIbIIIa inhibitors to the sole use of Gp IIbIIIa inhibitors before percutaneous coronary intervention (PCI) in patients presenting with acute ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Early reperfusion in STEMI is associated with improved outcomes. The use of reduced-dose thrombolytic and Gp IIbIIIa inhibitors combination before PCI in the setting of acute STEMI remains controversial. METHODS: We performed a literature search and identified randomized trials comparing the use of combination therapy-facilitated PCI versus PCI done with Gp IIbIIIa inhibitor alone. Included studies were reviewed to determine Thrombolysis in Myocardial Infarction (TIMI)-3 flow at baseline, major bleeding, 30-day mortality, TIMI-3 flow after PCI, and 30-day reinfarction. We performed a random-effect model meta-analysis. We quantified heterogeneity between studies with I2. A value >50% represents substantial heterogeneity. RESULTS: We identified 4 clinical trials randomizing 725 patients; 424 patients were pretreated with combination therapy before PCI, and 301 patients had Gp IIbIIIa inhibitor alone during PCI. Combination therapy-facilitated PCI was associated with a 2-fold increase in TIMI-3 flow upon arrival to the catheterization laboratory compared with the sole use of upstream Gp IIbIIIa inhibitors (192/390 patients [49%] versus 60/284 [21%]; relative risk [RR], 2.2; P < .00001). However, post-PCI TIMI-3 flow was similar between the 2 groups (279/319 patients [87%] versus 188/212 [88%]; RR, 0.99; P = .85). Major bleeding events significantly increased in the combination therapy group (40/420 patients [9.5%] versus 14/299 [4.7%]; RR, 2.2; P = .007). The 30-day mortality (15/424 patients [3.5%] versus 5/301 [1.7%]; RR, 1.47; P = .46) and 30-day reinfarction rate (5/424 patients [1.1%] versus 3/301 [1.0%]; RR, 0.96; P = .96) were similar in the 2 treatment groups. CONCLUSIONS: Awaiting the results of the ongoing clinical trials, the current cumulative evidence does not support the routine use of combination of reduced-dose thrombolytic and Gp IIbIIIa inhibitor therapy-facilitated PCI for the treatment of STEMI.