Clinical effectiveness of an outpatient pathway for low-risk chest pain emergency department visits.

BACKGROUND: Studies suggest that patients who present with atypical chest pain and are low or low-intermediate risk can safely undergo a rapid rule-out for cardiac ischemia with serial ECGs and cardiac biomarkers followed by additional testing as needed. We sought to evaluate a novel Emergency Department (ED) protocol for patients to undergo their additional functional testing as an outpatient. METHODS: Patients presenting to the ED with atypical chest pain, normal ECG, and negative cardiac troponin felt to be low risk were referred for outpatient stress testing within 72 hours of presentation as part of a pilot program. We analyzed test characteristics, length of stay, and 30-day return visits to ED in the pilot group and compared results to a similar cohort assessed in the ED by a traditional chest pain observation protocol. RESULTS: A total of 156 patients were included over a 5-month period with 29.5% not returning for testing. There was a 70% reduction in length of stay for outpatient stress test protocol patients. All-cause and cardiac return visits to the ED were not significantly different between the outpatient cohort and the traditional chest pain unit group and were reduced by 47 and 75%, respectively, in patients who completed their outpatient testing. The provisional injection protocol resulted in a 81% reduction in radiation exposure when compared to traditional MPI stress protocols due to a greater utilization of exercise treadmill tests without imaging. CONCLUSION: Outpatient stress testing is a reliable alternative to traditional chest pain observation with a significantly shorter length of stay, reduced healthcare costs, and improved radiation safety profile for patients when compared to traditional inpatient observation.

Caseous Calcification of Mitral Annulus: A Rare Monster Leading to Cerebrovascular Accident.

Caseous calcification of the mitral annulus (CCMA) is a rare variant of mitral annular calcification that maybe easily misdiagnosed or confused with an abscess, a tumor, or infective vegetation. The main pathophysiological mechanism leading to CCMA involves degeneration and calcium deposition on the mitral valve. We present a case of CCMA to help understand this clinical entity.

A Practical Approach to Lead Removal: Transvenous Tools and Techniques.

Removal of cardiovascular implantable electronic devices (CIED) is an important and growing field when managing patients presenting with device infections, need for upgrades, and lead failure. The complex skillset of transvenous lead removal is in high demand along with increasing numbers of implanted CIEDs. A systematic and comprehensive approach to this field, including knowledge of all available tools and vascular access techniques is essential for successful outcomes. This article serves as a practical resource presenting tools and techniques of transvenous lead extraction to help refine and master one's skill.

Randomized controlled trial of Amigo® robotically controlled versus manually controlled ablation of the cavo-tricuspid isthmus using a contact force ablation catheter.

BACKGROUND: Radiofrequency catheter ablation (RFCA) of the cavo-tricuspid isthmus (CTI) is a common treatment for atrial flutter (AFL). However, achieving bi-directional CTI conduction block may be difficult, partly due to catheter instability. OBJECTIVE: To evaluate the safety and efficacy of the Amigo® Remote Catheter System (RCS) compared to manual catheter manipulation, during CTI ablation for AFL. METHODS: Fifty patients (pts) were prospectively randomized to robotically (25 pts) versus manually (25 pts) controlled catheter manipulation during CTI ablation, using a force-contact sensing, irrigated ablation catheter. The primary outcome was recurrence of CTI conduction after a 30-min waiting period. Secondary outcomes included total ablation, procedure, and fluoroscopy times, contact force measurement, and catheter stability. RESULTS: Recurrence of CTI conduction 30 min after ablation was less with robotically (0/25) versus manually (6/25) controlled ablation (p = 0.023). Total ablation and procedure times to achieve persistent CTI block (6.7 ± 3 vs. 7.4 ± 2.5 min and 14.9 ± 7.5 vs. 15.2 ± 7 min, respectively) were not significantly different (p = 0.35 and p = 0.91, respectively). There was a non-significant trend toward a greater force time integral (FTI in gm/s) with robotically versus manually controlled CTI ablation (571 ± 278 vs. 471 ± 179, p = 0.13). Fluoroscopy time was longer with robotically versus manually controlled CTI ablation (6.8 ± 4.4 min vs. 3.8 ± 2.3 min, p = 0.0027). There were no complications in either group. CONCLUSION: Robotically controlled CTI ablation resulted in fewer acute recurrences of CTI conduction compared to manually controlled CTI ablation, and a trend toward higher FTI. The longer fluoroscopy time during robotically controlled ablation was likely due to a steep learning curve. TRIAL REGISTRATION: Clinicaltrials.gov Identifier: NCT02467179.

Intravascular Cooling Catheter-Related Venous Thromboembolism After Hypothermia: A Case Report and Review of the Literature.

Fifty-four year-old man with recent history of myocardial infarction and a percutaneous coronary intervention who suffered a ventricular fibrillation arrest at home. He was resuscitated in the field. His heart rhythm was in atrial fibrillation. The cardiac catheterization showed a patent stent from his previous myocardial infarction and no new occlusions. He subsequently underwent hypothermia protocol using the Alsius CoolGard 3000 Temperature Control System and Icy Catheter. Heparin drip was started for atrial fibrillation 36 hours after catheter insertion and became therapeutic 2 hours before the end of cooling maintenance phase. Heparin drip was stopped 4 hours into the rewarming phase because of spontaneous conversion to sinus rhythm. Subcutaneous heparin was resumed for deep venous thrombosis prophylaxis. He was extubated to room air after hypothermia protocol. The cooling catheter was removed 88 hours after insertion. Within 1 minute of catheter removal, his oxygen saturation dropped to 80%. Transthoracic echocardiogram showed a mobile thrombus in the right atrium prolapsing into the right ventricle. Computer tomography angiography of the chest confirmed a large saddle embolus. Ninety minutes later, patient went into cardiac arrest with pulseless electrical activity while he was being considered for surgical embolectomy, but he could not be resuscitated. The temporal relationship of the catheter removal and his acute clinical decompensation led to believe that this was an intravascular cooling catheter (ICC)-related event. Providers should be cognizant of the complications of central venous catheters such as thrombosis formation, as it could lead to fatal pulmonary embolism. Physicians should promote frequent assessment of the access site(s) during routine physical examinations and potentially use point of care vascular ultrasound in high-risk cases to rule out a catheter-associated thrombus before catheter removal.

The effect of rowing ergometry and resistive exercise on skeletal muscle structure and function during bed rest.

Exposure to microgravity causes functional and structural impairment of skeletal muscle. Current exercise regimens are time-consuming and insufficiently effective; an integrated countermeasure is needed that addresses musculoskeletal along with cardiovascular health. High-intensity, short-duration rowing ergometry and supplemental resistive strength exercise may achieve these goals. Twenty-seven healthy volunteers completed 5 wk of head-down-tilt bed rest (HDBR): 18 were randomized to exercise, 9 remained sedentary. Exercise consisted of rowing ergometry 6 days/wk, including interval training, and supplemental strength training 2 days/wk. Measurements before and after HDBR and following reambulation included assessment of strength, skeletal muscle volume (MRI), and muscle metabolism (magnetic resonance spectroscopy); quadriceps muscle biopsies were obtained to assess muscle fiber types, capillarization, and oxidative capacity. Sedentary bed rest (BR) led to decreased muscle volume (quadriceps: -9 ± 4%, P < 0.001; plantar flexors: -19 ± 6%, P < 0.001). Exercise (ExBR) reduced atrophy in the quadriceps (-5 ± 4%, interaction P = 0.018) and calf muscle, although to a lesser degree (-14 ± 6%, interaction P = 0.076). Knee extensor and plantar flexor strength was impaired by BR (-14 ± 15%, P = 0.014 and -22 ± 7%, P = 0.001) but preserved by ExBR (-4 ± 13%, P = 0.238 and +13 ± 28%, P = 0.011). Metabolic capacity, as assessed by maximal O2 consumption, (31)P-MRS, and oxidative chain enzyme activity, was impaired in BR but stable or improved in ExBR. Reambulation reversed the negative impact of BR. High-intensity, short-duration rowing and supplemental strength training effectively preserved skeletal muscle function and structure while partially preventing atrophy in key antigravity muscles. Due to its integrated cardiovascular benefits, rowing ergometry could be a primary component of exercise prescriptions for astronauts or patients suffering from severe deconditioning.

Day/night variability in blood pressure: influence of posture and physical activity.

BACKGROUND: Blood pressure (BP) is highest during the day and lowest at night. Absence of this rhythm is a predictor of cardiovascular morbidity and mortality. Contributions of changes in posture and physical activity to the 24-hour day/night rhythm in BP are not well understood. We hypothesized that postural changes and physical activity contribute substantially to the day/night rhythm in BP. METHODS: Fourteen healthy, sedentary, nonobese, normotensive men (aged 19-50 years) each completed an ambulatory and a bed rest condition during which BP was measured every 30-60 minutes for 24 hours. When ambulatory, subjects followed their usual routines without restrictions to capture the "normal" condition. During bed rest, subjects were constantly confined to bed in a 6-degree head-down position; therefore posture was constant, and physical activity was minimized. Two subjects were excluded from analysis because of irregular sleep timing. RESULTS: The systolic and diastolic BP reduction during the sleep period was similar in ambulatory (-11±2mmHg/-8±1mmHg) and bed rest conditions (-8±3mmHg/-4±2mmHg; P = 0.38/P = 0.12). The morning surge in diastolic BP was attenuated during bed rest (P = 0.001), and there was a statistical trend for the same effect in systolic BP (P = 0.06). CONCLUSIONS: A substantial proportion of the 24-hour BP rhythm remained during bed rest, indicating that typical daily changes in posture and/or physical activity do not entirely explain 24-hour BP variation under normal ambulatory conditions. However, the morning BP increase was attenuated during bed rest, suggesting that the adoption of an upright posture and/or physical activity in the morning contributes to the morning BP surge.

Effect of rowing ergometry and oral volume loading on cardiovascular structure and function during bed rest.

This study examined the effectiveness of a short-duration but high-intensity exercise countermeasure in combination with a novel oral volume load in preventing bed rest deconditioning and orthostatic intolerance. Bed rest reduces work capacity and orthostatic tolerance due in part to cardiac atrophy and decreased stroke volume. Twenty seven healthy subjects completed 5 wk of -6 degree head down bed rest. Eighteen were randomized to daily rowing ergometry and biweekly strength training while nine remained sedentary. Measurements included cardiac mass, invasive pressure-volume relations, maximal upright exercise capacity, and orthostatic tolerance. Before post-bed rest orthostatic tolerance and exercise testing, nine exercise subjects were given 2 days of fludrocortisone and increased salt. Sedentary bed rest led to cardiac atrophy (125 ± 23 vs. 115 ± 20 g; P < 0.001); however, exercise preserved cardiac mass (128 ± 38 vs. 137 ± 34 g; P = 0.002). Exercise training preserved left ventricular chamber compliance, whereas sedentary bed rest increased stiffness (180 ± 170%, P = 0.032). Orthostatic tolerance was preserved only when exercise was combined with volume loading (-10 ± 22%, P = 0.169) but not with exercise (-14 ± 43%, P = 0.047) or sedentary bed rest (-24 ± 26%, P = 0.035) alone. Rowing and supplemental strength training prevent cardiovascular deconditioning during prolonged bed rest. When combined with an oral volume load, orthostatic tolerance is also preserved. This combined countermeasure may be an ideal strategy for prolonged spaceflight, or patients with orthostatic intolerance.

Congestive heart failure with preserved ejection fraction is associated with severely impaired dynamic Starling mechanism.

Sedentary aging leads to increased cardiovascular stiffening, which can be ameliorated by sufficient amounts of lifelong exercise training. An even more extreme form of cardiovascular stiffening can be seen in heart failure with preserved ejection fraction (HFpEF), which comprises ~40~50% of elderly patients diagnosed with congestive heart failure. There are two major interrelated hypotheses proposed to explain heart failure in these patients: 1) increased left ventricular (LV) diastolic stiffness and 2) increased arterial stiffening. The beat-to-beat dynamic Starling mechanism, which is impaired with healthy human aging, reflects the interaction between ventricular and arterial stiffness and thus may provide a link between these two mechanisms underlying HFpEF. Spectral transfer function analysis was applied between beat-to-beat changes in LV end-diastolic pressure (LVEDP; estimated from pulmonary artery diastolic pressure with a right heart catheter) and stroke volume (SV) index. The dynamic Starling mechanism (transfer function gain between LVEDP and the SV index) was impaired in HFpEF patients (n = 10) compared with healthy age-matched controls (n = 12) (HFpEF: 0.23 ± 0.10 ml·m⁻²·mmHg⁻¹ and control: 0.37 ± 0.11 ml·m⁻²·mmHg⁻¹, means ± SD, P = 0.008). There was also a markedly increased (3-fold) fluctuation of LV filling pressures (power spectral density of LVEDP) in HFpEF patients, which may predispose to pulmonary edema due to intermittent exposure to higher pulmonary capillary pressure (HFpEF: 12.2 ± 10.4 mmHg² and control: 3.8 ± 2.9 mmHg², P = 0.014). An impaired dynamic Starling mechanism, even more extreme than that observed with healthy aging, is associated with marked breath-by-breath LVEDP variability and may reflect advanced ventricular and arterial stiffness in HFpEF, possibly contributing to reduced forward output and pulmonary congestion.