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Objectives In a nonclinical trial setting, we sought to determine the proportion of individuals with coronary artery disease (CAD) with optimal risk factor levels based on the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation) trial. Background In the COURAGE trial, the addition of percutaneous coronary intervention (PCI) to optimal medical therapy did not reduce the risk of death or myocardial infarction in stable CAD patients but resulted in more revascularization procedures. Methods The REGARDS (REasons for Geographic And Racial Differences in Stroke) study is a national prospective cohort study of 30,239 African-American and white community-dwelling individuals older than 45 years of age who enrolled in 2003 through 2007. We calculated the proportion of 3,167 participants with self-reported CAD meeting 7 risk factor goals based on the COURAGE trial: 1) aspirin use; 2) systolic blood pressure 40 mg/dl, and triglycerides Results The mean age of participants was 69 ± 9 years; 33% were African American and 35% were female. Overall, the median number of goals met was 4. Less than one-fourth met ≥5 of the 7 goals, and 16% met all 3 goals for aspirin, blood pressure, and low-density lipoprotein cholesterol. Older age, white race, higher income, more education, and higher physical functioning were independently associated with meeting more goals. Conclusions There is substantial room for improvement in risk factor reduction among U.S. individuals with CAD.

A 57-year-old woman with idiopathic premature ventricular contractions (PVCs) exhibiting a left bundle branch block and left inferior axis QRS morphology underwent electrophysiological testing. Mapping revealed that the earliest ventricular activation times during the PVCs recorded on either side of the interventricular septum were the same and no excellent pace maps were reproduced at these sites. Successful radiofrequency catheter ablation was achieved in the right ventricular septum adjacent to the recording site of the His bundle electrogram. These findings suggested that the origin of this PVC was located in the intraventricular septum rather than the endocardial surface.

Soon after an upgrade from a single-chamber implantable cardioverter-defibrillator (ICD) to cardiac resynchronization therapy (CRT) with an ICD, a 64-year-old man with non-ischaemic cardiomyopathy began to have increasingly frequent ICD shocks for slow ventricular tachycardia (VT). At electrophysiological study, no clinical VT was induced by endocardial right ventricular pacing, but was easily induced by epicardial left ventricular (LV) pacing via a subxiphoid pericardial approach. The VT was successfully ablated on the LV epicardial surface. This case suggests that epicardial catheter ablation may be an alternative for managing CRT-induced proarrhythmias without the inactivation of LV pacing.

IVTs Arising from the LV Anterior Papillary Muscle. Introduction: Focal ventricular arrhythmias (VAs) have been reported to arise from the posterior papillary muscle in the left ventricle (LV). We report a distinct subgroup of idiopathic VAs arising from the anterior papillary muscle (APM) in the LV. Methods and Results: We studied 432 consecutive patients undergoing catheter ablation for VAs based on a focal mechanism. Six patients were identified with ventricular tachycardia (VT, n = 1) or premature ventricular contractions (PVCs, n = 5) with the earliest site of ventricular activation localized to the base (n = 3) or middle portion (n = 3) of the LV APM. No Purkinje potentials were recorded at the ablation site during sinus rhythm or the VAs. All patients had a normal baseline electrocardiogram and normal LV systolic function. The VAs exhibited a right bundle branch block (RBBB) and right inferior axis (RIA) QRS morphology in all patients. Oral verapamil and/or Na + channel blockers failed to control the VAs in 4 patients. VT was not inducible by programmed electrical stimulation in any of the patients. In 4 patients, radiofrequency current with an irrigated or conventional 8-mm-tip ablation catheter was required to achieve a lasting success. Two patients had recurrent PVCs after a conventional radiofrequency ablation with a 4-mm-tip ablation catheter had initially suppressed the arrhythmia. Conclusions: VAs may arise from the base or middle portion of the APM and are characterized by an RBBB and RIA QRS morphology and focal mechanism. Catheter ablation of APM VAs is typically challenging, and creation of a deep radiofrequency lesion may be necessary for long-term success.

Macro-Reentrant ARVC epi-VT with a Focal Endo-Activation. A 55-year-old man with arrhythmogenic right ventricular cardiomyopathy underwent catheter ablation of ventricular tachycardia (VT) with left bundle branch block and left superior axis QRS morphology with an early precordial transition. Endocardial mapping during the VT revealed a focal activation pattern from a small region of low voltage in the left ventricular (LV) septum. Despite earliest endocardial activation in the LV septum, epicardial mapping demonstrated a macro-reentrant circuit with successful catheter ablation at an inferior peritricuspid annular site. Activation from the reentrant circuit propagated through the scar area in the epicardial right ventricle to the remote endocardial LV breakout site.

A 66-year-old man with cor triatriatum sinister underwent pulmonary vein (PV) isolation (PVI) for atrial fibrillation (AF) twice because of AF recurrence. Different transseptal approaches into the anterior chamber receiving the left atrial appendage and posterior chamber receiving the PVs, were achieved in two sessions. PVI of the left PVs and right superior PV was challenging via the anterior chamber, whereas PVI of the right inferior PV was challenging via the posterior chamber because of the disturbance of the membrane. Therefore, an intentional transseptal catheterization into the more appropriate chamber may be necessary for PVI in a cor triatriatum sinister.

Background— During resuscitation, fibrillation often recurs. In swine, we studied refibrillation after long-duration ventricular fibrillation, investigating an association with chest compressions (CCs). Methods and Results— In protocol A, 47 episodes of long-duration ventricular fibrillation lasting at least 2.5 minutes were induced in 8 animals. After defibrillation, CCs were required for 35 episodes and delivered with a pneumatic device (Lucas cardiopulmonary resuscitation). In 9 episodes, refibrillation occurred within 2 seconds of CC initiation (group 1) and in 26 episodes, CCs were delivered without refibrillation (group 2). From the ECG and intracardiac electrodes, the RR interval preceding CCs, the shortest cycle length during the first 2 CCs (short), and the preceding cycle length (long) were measured. A similar study was conducted in 3 more animals without intracardiac catheters (protocol B). In protocol A, the mean RR before CC was 665�292 ms in group 1 and 769�316 in group 2. CCs stimulated ventricular beats in all 35 episodes. The short and long intervals were shorter in group 1 (215�31 and 552�210 ms) than in group 2 (402�153 and 699�147 ms) ( P =0.009 and P =0.04, respectively). The prematurity index (short/RR) was lower in group 1 than in group 2 (0.35�0.09 vs 0.58�0.21; P Conclusions— Under some conditions, CC during resuscitation can stimulate the ventricles and initiate ventricular fibrillation by a long-short sequence.

Genetic testing is increasingly becoming possible for diagnosis, susceptibility testing, and prognostication in cardiovascular medicine. The practicing cardiologist, therefore, needs to be familiar with the clinical utilities and limitations of genetic testing. This review explores the major approaches to genetic testing and issues in test interpretation. Specific applications to cardiovascular diseases, including coronary artery disease, cardiomyopathies, cardiac arrhythmias, and pulmonary arterial hypertension are discussed.

An 81-year-old woman was admitted for symptomatic bradycardia. On admission, the ECG exhibited QRS alternans, narrow QRS complex and left bundle branch block with 2:1 AV block. The patient soon had complete AV block and underwent a pacemaker implantation. An appropriate mechanism for explaining those ECG findings might be 4:1 conduction over the left bundle branch and 2:1 conduction over the right bundle branch. An ECG pattern exhibiting QRS alternans with a narrow QRS complex and bundle branch block with 2:1 AV block may suggest the coexistence of both bundle branch blocks and a high risk of complete AV block.

To compare the clinical utility of bone marrow biopsy and culture specimens with blood cultures for mycobacterial and fungal infections among human immunodeficiency virus (HIV)-infected patients.All bone marrow biopsies obtained from HIV-infected patients at the University of Alabama at Birmingham (UAB) Medical Center during 1993 to 1995 were blindly reviewed in a standardized format. Bone marrow culture results and blood culture results obtained within 6 weeks of each bone marrow study were compiled. Medical records were reviewed to determine indications for performing bone marrow biopsies, empiric or prophylactic antimicrobial therapies preceding the biopsy, and CD4 counts.Eighty-two bone marrow studies were obtained from 76 patients. Most were performed during the evaluation of fever, cytopenia, or weight loss. Of 55 bone marrow mycobacterial cultures, 13 yielded Mycobacterium avium complex (MAC) and 2 yielded M tuberculosis (MTB). Of 51 bone marrow fungal cultures performed, 2 yielded Cryptococcus neoformans and 1 Histoplasma capsulatum. All patients with a bone marrow culture positive for MAC had a CD4 count of 20 cells/mm3 or less. The mean CD4 count in this group (+/-95% confidence interval) (8+/-3 cells/mm3) was lower than that of culture-negative cases (41+/-25 cells/mm3); P0.015). When bone marrow cultures and mycobacterial blood cultures were concurrently obtained, results were usually in agreement between the two sites. The mean time until the report of positive mycobacterial bone marrow cultures (22+/-5 days) was similar to that for blood cultures (24+/-3 days). Most (84%) patients with multiple mycobacterial cultures had completely concordant results (all positive or all negative). When blood or bone marrow culture yielded mycobacteria, only 29% of the corresponding bone marrow examinations revealed stainable acid-fast bacilli (AFB). In contrast, all 3 cases with positive fungal bone marrow cultures also had stainable organisms on histologic examination.The combined use of bone marrow biopsy and culture as well as blood cultures provide the maximum diagnostic yield when evaluating patients with AIDS for mycobacterial or fungal infections. However, when mycobacterial infections were diagnosed, bone marrow results seldom provided more immediate or specific information than lysis centrifugation blood cultures. A single lysis centrifugation blood culture should be the first step in the routine evaluation of HIV-infected patients when disseminated MAC infection is suspected.

External mechanical forces can cause ventricular capture and fibrillation (i.e., commotio cordis). In animals, we showed that chest compressions (CCs) can also cause the phenomenon. The aim of the present study was to determine whether ventricular capture by CCs occurs in humans. Electronic rhythm strips were analyzed in 31 cases of out-of-hospital cardiac arrest. The timing of the CCs was identified from the changes in thoracic impedance between the defibrillator pads. Ventricular capture was defined as QRS complexes of similar morphology occurring intermittently but synchronized with the CC artifact and impedance waveform. Only intermittent ventricular capture was identified to avoid misclassifying constant motion artifacts or intrinsic rhythm as ventricular capture. Of the 29 patients who received CCs for ≥1 minute, minimal or stable motion artifact was present in 24. Intermittent ventricular capture was found in 7 of the 24 patients. In the patients with ventricular capture, the number of ventricular activations (from ventricular capture and native beats) was greater during the CCs than when the CCs was not being performed (18 ± 8.9 vs 9.7 ± 4.0 activations in 15 seconds, p = 0.01). However, in patients without ventricular capture, they were similar (6.8 ± 8.2 vs 7.2 ± 8.8 activations in 15 seconds, p = 0.47). Refibrillation occurred in 22 patients; it began during the CCs in 16 and closely following their initiation in 3. In conclusion, CCs during cardiopulmonary resuscitation can electrically stimulate the heart. Additional studies evaluating the effect of ventricular capture on cardiopulmonary resuscitation outcomes, its relation to refibrillation, and methods to prevent or time ventricular capture by CCs are warranted.

Limited Response to CRT in Patients with RVD. Introduction: Patients with left ventricular dysfunction (LVD) and LV dyssynchrony may respond to cardiac resynchronization therapy (CRT). However, right ventricular dysfunction (RVD) is a predictor of decreased survival in patients with LVD, and its influence on clinical response to CRT is unknown. The purpose of this study was to examine the effect of RVD on the clinical response to CRT. Methods and Results: A retrospective cohort of consecutive patients who underwent implantation of a CRT implantable cardioverter-defibrillator (ICD) were included and deemed to have RVD based on a RV ejection fraction

Ventricular fibrillation (VF), despite its declining incidence as a cause of sudden cardiac death, is still a major health problem. The underlying mechanisms for the maintenance of VF are still disputed. Studies suggest that VF is unlikely one static mechanism but rather a dynamic process of electrical derangement that changes with duration. The 2 principal proposed mechanisms of VF are multiple wavelets and mother rotors. Most studies of these proposed mechanisms for VF maintenance have been during the first minute of VF. However, the time to external defibrillation in the community and pre-hospital settings, where the majority of sudden cardiac death occurs, ranges from 4 to 10 min and the time to defibrillation seems crucial because the odds of survival worsen with delay. Recent studies during the first 10 min of VF suggest that Purkinje fibers are important in maintaining VF after the first 1 to 2 min, either as a part of a reentrant circuit or as a source of focal activations.

A 61-year-old man with a remote posterior myocardial infarction underwent electrophysiological testing for a ventricular tachycardia (VT) storm. Repeated cardioversions terminated the VT with immediate resumption after one sinus beat. Pacing neither terminated the VT nor demonstrated transient entrainment. Echocardiographically guided electroanatomic mapping revealed a centrifugal activation from the septal mid-apical region of the left ventricle on the septal portion of the posterior papillary muscle where a high frequency potential was observed within the local ventricular electrogram. Irrigated radiofrequency current at this site eliminated the VT. This case suggested that papillary muscles may be a target for catheter ablation of electrical storms after myocardial infarctions.

Endocardial mapping has suggested that Purkinje fibers may play a role in the maintenance of long-duration ventricular fibrillation (LDVF). To determine the influence of Purkinje fibers on LDVF, we chemically ablated the Purkinje system with Lugol solution and recorded endocardial and transmural activation during LDVF. Dog hearts were isolated and perfused, and the ventricular endocardium was exposed and treated with Lugol solution ( n = 6) or normal Tyrode solution as a control ( n = 6). The left anterior papillary muscle endocardium was mapped with a 504-electrode (21 × 24) plaque with electrodes spaced 1 mm apart. Transmural activation was recorded with a six-electrode plunge needle on each side of the plaque. Ventricular fibrillation (VF) was induced, and perfusion was halted. LDVF spontaneously terminated sooner in Lugol-ablated hearts than in control hearts (4.9 ± 1.5 vs. 9.2 ± 3.2 min, P = 0.01). After termination of VF, both the control and Lugol hearts were typically excitable, but only short episodes of VF could be reinduced. Endocardial activation rates were similar during the first 2 min of LDVF for Lugol-ablated and control hearts but were significantly slower in Lugol hearts by 3 min. In control hearts, the endocardium activated more rapidly than the epicardium after 4 min of LDVF with wave fronts propagating most often from the endocardium to epicardium. No difference in transmural activation rate or wave front direction was observed in Lugol hearts. Ablation of the subendocardium hastens VF spontaneous termination and alters VF activation sequences, suggesting that Purkinje fibers are important in the maintenance of LDVF.

Background Cycle length (CL) increases as ventricular fibrillation (VF) progresses. Objective The purpose of this study was to test the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased postrepolarization refractoriness. Methods In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V max ), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DI min ). In two animals, rapid pacing was performed to gauge refractoriness. Results As VF progressed, CL, DI, and DI min increased ( P max , and APA decreased ( P min was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque. Conclusion Increasing CL in VF is due to increased DI and not APD, which shortens. The increase in DI min over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V max secondary to global ischemia caused by VF.

Alcohol septal ablation (ASA) as a treatment for obstructive hypertrophic cardiomyopathy produces septal infarction. There is a concern that such infarcts could be detrimental. Changes in the size of these infarcts by serial perfusion testing have not been studied. We performed resting serial-gated single-photon emission computed tomographic myocardial perfusion imaging in 30 patients (age 51+/-17 years, 57% were women) who had ASA between September 2003 and March 2007 before, 2+/-0.8 days (early), and 8.4+/-6.9 months (late) after ASA. Patients were also followed clinically and with serial 2-dimensional echocardiography. New York Heart Association class decreased from 3.50+/-0.51 before to 1.14+/-0.36 (p0.0001) 3 months after ASA. The left ventricular (LV) outflow gradient (by Doppler echocardiography) decreased from 63+/-32 mm Hg before to 28+/-23 mm Hg after ASA (p0.005). None of the patients had perfusion defects at rest before ASA. After ASA, perfusion defect size, involving the basal septum, decreased from 9.4+/-5.8% early to 5.2+/-4.2% of LV myocardium late after ASA (p0.001). There were no changes in LV size and ejection fraction after ASA. In conclusion, ASA produces small basal ventricular septal infarcts (resting perfusion abnormality) involving10% of the LV myocardium (including ventricular septum). There is a significant reduction in the perfusion abnormality late after ASA without an increase in LV outflow obstruction or recurrence of symptoms.

Background— The roles of Purkinje fibers (PFs) and focal wave fronts, if any, in the maintenance of ventricular fibrillation (VF) are unknown. If PFs are involved in VF maintenance, it should be possible to map wave fronts propagating from PFs into the working ventricular myocardium during VF. If wave fronts ever arise focally during VF, it should be possible to map them appearing de novo. Methods and Results— Six canine hearts were isolated, and the left main coronary artery was cannulated and perfused. The left ventricular cavity was exposed, which allowed direct endocardial mapping of the anterior papillary muscle insertion. Nonperfused VF was induced, and 6 segments of data, each 5 seconds long, were analyzed during 10 minutes of VF. During 36 segments of data that were analyzed, 1018 PF or focal wave fronts of activation were identified. In 534 wave fronts, activation was mapped propagating from working ventricular myocardium to PF. In 142 wave fronts, activation was mapped propagating from PF to working ventricular myocardium. In 342 wave fronts, activation was mapped arising focally. More than 1 of these 3 patterns could occur in the same wave front. Conclusions— PFs are highly active throughout the first 10 minutes of VF. In addition to retrograde propagation from the working ventricular myocardium to PFs, antegrade propagation occurs from PFs to working ventricular myocardium, which suggests PFs are important in VF maintenance. Prior plunge needle recordings in dogs indicate activation propagates from the endocardium toward the epicardium after 1 minute of VF, which suggests that focal sites on the endocardium may represent foci and not breakthrough. If so, in addition to reentry, abnormal automaticity or triggered activity may also occur during VF.

Background: We sought to describe the proportion of acute ischemic stroke admissions for very old patients (≧85 years), compare the characteristics of very old versus younger patients and identify factors among very old patients associated with adverse outcomes. Methods: The 2000 Healthcare Cost and Utilization Project data included acute ischemic stroke hospitalizations for patients ≧45 years. The combined outcome was in-hospital mortality or discharge to a long-term care facility. Results: Among 15,020 stroke hospitalizations, 20.4% were for very old patients. The outcome rate was higher in hospitalizations for very old patients (2,176/3,058, 71.2%; versus 5,748/11,962, 48%; p < 0.0001). More hospitalizations for very old patients were for women (73.5 versus 55.1%; p < 0.0001), fewer for Blacks (6.1 versus 12.3%; p < 0.0001) and fewer at teaching hospitals (30.4 versus 36.2%; p < 0.0001). Among very old patients, factors that were independently associated with the outcome included: age [years; adjusted OR = 1.02 (95% CI = 1.000–1.05)], female gender [1.4 (1.18–1.68)], atrial fibrillation [1.37 (1.15–1.63)], acute myocardial infarction [1.68 (1.20–2.35)], respiratory failure [3.59 (1.60–8.05)] and teaching hospital admission [0.82 (0.69–0.98)]. Similar results were observed in the hospitalizations for younger patients. The adjusted OR for the outcome displayed geographic disparities in both age groups, but the pattern of the geographic variation was not similar between the two age groups. Conclusions: The very old constitute a substantial proportion of stroke hospitalizations. Hospitalizations for very old patients are more likely to end in death or discharge to a long-term care facility than hospitalizations for younger patients. The pattern of geographic disparity in poststroke adverse outcomes differs between younger and very old patients.

Background Many processes of care have been proposed as metrics to evaluate stroke care. We sought to identify processes of stroke care that are associated with improved patient outcomes after adjustment for both patient characteristics and other process measures. Methods This retrospective cohort study included patients 18 years or older with an ischemic stroke or transient ischemic attack (TIA) onset no more than 2 days before admission and a neurologic deficit on admission. Patients were excluded if they resided in a skilled nursing facility, were already admitted to the hospital at stroke onset, or were transferred from another acute-care facility. The combined outcome included in-hospital mortality, discharge to hospice, or discharge to a skilled nursing facility. Seven processes of stroke care were evaluated: fever management, hypoxia management, blood pressure management, neurologic evaluation, swallowing evaluation, deep vein thrombosis (DVT) prophylaxis, and early mobilization. Risk adjustment included age, comorbidity (medical history), concomitant medical illness present at admission, preadmission symptom course, prestroke functional status, code status, stroke severity, nonneurologic status, modified APACHE (Acute Physiology and Chronic Health Evaluation) III score, and admission brain imaging findings. Results Among 1487 patients, the outcome was observed in 239 (16%). Three processes of care were independently associated with an improvement in the outcome after adjustment: swallowing evaluation (adjusted odds ratio [OR], 0.64; 95% confidence interval [CI], 0.43-0.94); DVT prophylaxis (adjusted OR, 0.60; 95% CI, 0.37-0.96); and treating all episodes of hypoxia with supplemental oxygen (adjusted OR, 0.26; 95% CI, 0.09-0.73). Conclusion Outcomes among patients with ischemic stroke or TIA can be improved by attention to swallowing function, DVT prophylaxis, and treatment of hypoxia.