Right Ventricular Myocardial Infarction-A Tale of Two Ventricles: JACC Focus Seminar 1/5.

Right ventricular infarction (RVI) complicates 50% of cases of acute inferior ST-segment elevation myocardial infarction, and is associated with high in-hospital morbidity and mortality. Ischemic right ventricular (RV) systolic dysfunction decreases left ventricular preload delivery, resulting in low-output hypotension with clear lungs, and disproportionate right heart failure. RV systolic performance is generated by left ventricular contractile contributions mediated by the septum. Augmented right atrial contraction optimizes RV performance, whereas very proximal occlusions induce right atrial ischemia exacerbating hemodynamic compromise. RVI is associated with vagal mediated bradyarrhythmias, both during acute occlusion and abruptly with reperfusion. The ischemic dilated RV is also prone to malignant ventricular arrhythmias. Nevertheless, RV is remarkably resistant to infarction. Reperfusion facilitates RV recovery, even after prolonged occlusion and in patients with severe shock. However, in some cases hemodynamic compromise persists, necessitating pharmacological and mechanical circulatory support with dedicated RV assist devices as a "bridge to recovery."

Comprehensive radiation shield minimizes operator radiation exposure in coronary and structural heart procedures.

OBJECTIVES: This study evaluated the efficacy of a novel comprehensive shield designed to minimize radiation exposure (RE) to Physicians performing coronary and structural heart procedures. BACKGROUND: The Protego™ radiation shielding system (Image Diagnostics Inc., Fitchburg, Ma) is designed to provide comprehensive protection from RE and has been State certified sufficient to allow operators to perform procedures without orthopedically burdensome lead aprons. METHODS: This single center two-group cohort study assessed the efficacy of this shield in a large number of cardiac procedures (coronary and structural), comparing operator RE compared to standard protection methods (personal lead apparel and "drop down" shield). RESULTS: The Protego™ system reduced operator RE by 99 % compared to Standard Protection. RE was significantly lower at both "Head" level by thyroid median dose 0.0 (0.0, 0,0) vs 5.7 (2.9, 8.2) µSv (p < 0.001), as well as waist dose 0.0 (0.0, 0.0) vs 10.0 (5.0, 16.6) µSv (p < 0.001). "Zero" Total RE was documented by Raysafe™ in 64 % (n = 32) of TAVR cases and 73.2 % (n = 183) of the coronary cases utilizing Protego™. In contrast, standard protection did not achieve "Zero" exposure in a single case. These dramatic differences in RE were achieved despite higher fluoroscopy times in the Protego™ arm (11.9 ± 8.6 vs 14.3 ± 12.5 min, p = 0.015). Per case procedural exposure measured by Dose Area Product was higher in the Protego™ group compared to standard protection (115.4 ± 139.2 vs 74.9 ± 69.3, p < 0.001). CONCLUSION: The Protego™ shield provides total body RE protection for operators performing both coronary and structural heart procedures. This shield allows procedural performance without the need for personal lead aprons and has potential to reduce catheterization laboratory occupational health hazards.

Valve-in-Mitral Annular Calcification Transcatheter Mitral Valve Replacement After Thrombosis of Extracardiac Valved Conduit.

We report a patient with severe mitral annular calcification, mitral stenosis/regurgitation, hypertrophic obstructive cardiomyopathy, and subaortic membrane treated with valved left atrium-left ventricle conduit, septal myectomy, and membrane resection. Subsequent thrombosis of the conduit prompted successful valve-in- mitral annular calcification transcatheter mitral valve replacement and laceration of the anterior mitral leaflet to prevent outflow obstruction. (Level of Difficulty: Advanced.).

Hemodynamic compromise in pulmonary embolism: "A tale of two ventricles".

In acute pulmonary embolism (PE), low cardiac output (CO)-hypotension results from disparate ventricular conditions: The left ventricle (LV) is under-filled and contracting vigorously, whereas the right ventricle (RV) is failing and dilated. The proximate cause of LV preload deprivation is thrombus-induced pulmonary vascular obstruction; abruptly increased pulmonary vascular resistance (PVR) induces acute RV systolic dysfunction which further compromises trans-pulmonary flow. "Escalation of Care" interventions (thrombolytics and aspiration thrombectomy) improve systemic hemodynamics by increasing LV preload delivery directly by reducing PVR and indirectly by relief of the strained failing RV.

Disparate impact of severe aortic and mitral regurgitation on left ventricular dilation.

In asymptomatic severe aortic (AR) and mitral regurgitation (MR), left ventricular (LV) dimension criteria were established to guide timing of valve replacement to prevent irreversible LV dysfunction. Given both lesions are primary LV volume overload ''leaks'', it might be expected that both lesions would induce similar impact on the LV and result in equivalent dimension criteria for intervention. However, the dimension-based intervention criteria for AR versus MR (developed through natural history studies), differ markedly. The pathophysiological foundations for such discordance have neither been fully elucidated nor emphasized. This case-based treatise compares the two regurgitant lesions with respect to: (a) ''total regurgitant circuits''; (b) ''driving pressures'' resulting in LV volume overload from each respective ''leak''; and (c) volume and afterload wall stresses imposed on the LV.Key points The ''total circuits'' of volume overload differ: The AR circuit includes the LV and systemic vasculature, whereas MR includes the LV ejecting into the left atrium/pulmonary veins and systemic circulation. The ''driving pressure'' of regurgitation and afterload are high with AR and low with MR. Differing ''total circuits'' and ''driving pressures'' impose disparate wall stresses upon the LV. Parallel and serial sarcomere replication occurs in AR, while only serial replication occurs in MR. It therefore follows that for regurgitation of similar severities, AR results in greater LV dilation at the point of irreversible myocardial dysfunction compared to MR. These considerations may explain, at least in part, the disparate dimension criteria employed for valve intervention for severe AR vs MR.

Impella RP for treatment of right ventricular shock: Appropriate unloading never gets old.

Rapid restoration of hemodynamics is key to successful shock management. The failing right ventricular (RV) is resilient and recovers if hemodynamics are supported while the underlying insulting cause is alleviated. Inotropic/vasopressor drugs constitute a "double-edged sword" that augment hemodynamics, but exacerbate myocardial and multiorgan injury. Impella RP mechanical support for RV shock stabilizes hemodynamics and is associated with favorable clinical outcomes.

Hemodynamic principles of prosthetic aortic valve evaluation in the transcatheter aortic valve replacement era.

Evaluating the hemodynamic performance of aortic valve prostheses has relied primarily on echocardiography. This involves calculating the trans-prosthetic valve mean gradient (MG) and aortic valve area (AVA), and assessing for valvular and paravalvular regurgitation in a fashion similar to the native aortic valve. In conjunction with other echocardiographic and nonechocardiographic parameters, MG and AVA are used to distinguish between prosthesis stenosis, prosthesis patient mismatch, pressure recovery, increased flow, and measurement errors. This review will discuss the principles and limitations of echocardiographic evaluation of aortic valve prosthesis following surgical, and transcatheter aortic valve replacement and in comparison to invasive hemodynamics through illustrative clinical cases.

2-Year Outcomes After Stenting of Lipid-Rich and Nonrich Coronary Plaques.

BACKGROUND: Autopsy studies suggest that implanting stents in lipid-rich plaque (LRP) may be associated with adverse outcomes. OBJECTIVES: The purpose of this study was to evaluate the association between LRP detected by near-infrared spectroscopy (NIRS) and clinical outcomes in patients with coronary artery disease treated with contemporary drug-eluting stents. METHODS: In this prospective, multicenter registry, NIRS was performed in patients undergoing coronary angiography and possible percutaneous coronary intervention (PCI). Lipid core burden index (LCBI) was calculated as the fraction of pixels with the probability of LRP >0.6 within a region of interest. MaxLCBI4mm was defined as the maximum LCBI within any 4-mm-long segment. Major adverse cardiac events (MACE) included cardiac death, myocardial infarction, definite or probable stent thrombosis, or unplanned revascularization or rehospitalization for progressive angina or unstable angina. Events were subcategorized as culprit (treated) lesion-related, nonculprit (untreated) lesion-related, or indeterminate. RESULTS: Among 1,999 patients who were enrolled in the COLOR (Chemometric Observations of Lipid Core Plaques of Interest in Native Coronary Arteries Registry), PCI was performed in 1,621 patients and MACE occurred in 18.0% of patients, of which 8.3% were culprit lesion-related, 10.7% were nonculprit lesion-related, and 3.1% were indeterminate during 2-year follow-up. Complications from NIRS imaging occurred in 9 patients (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass. Pre-PCI NIRS imaging was obtained in 1,189 patients, and the 2-year rate of culprit lesion-related MACE was not significantly associated with maxLCBI4mm (hazard ratio of maxLCBI4mm per 100: 1.06; 95% confidence interval: 0.96 to 1.17; p = 0.28) after adjusting clinical and procedural factors. CONCLUSIONS: Following PCI with contemporary drug-eluting stents, stent implantation in NIRS-defined LRPs was not associated with increased periprocedural or late adverse outcomes compared with those without significant lipid.

Transcranial Random Noise Stimulation for the Acute Treatment of Depression: A Randomized Controlled Trial.

BACKGROUND: Transcranial electrical stimulation has broad potential as a treatment for depression. Transcranial random noise stimulation, which delivers randomly fluctuating current intensities, may have greater cortical excitatory effects compared with other forms of transcranial electrical stimulation. We therefore aimed to investigate the antidepressant efficacy of transcranial random noise stimulation. METHODS: Depressed participants were randomly assigned by computer number generator to receive 20 sessions of either active or sham transcranial random noise stimulation over 4 weeks in a double-blinded, parallel group randomized-controlled trial. Transcranial random noise stimulation was delivered for 30 minutes with a direct current offset of 2 mA and a random noise range of 2 mA. Primary analyses assessed changes in depression severity using the Montgomery-Asperg Depression Rating Scale. Neuroplasticity, neuropsychological, and safety outcomes were analyzed as secondary measures. RESULTS: Sixty-nine participants were randomized, of which 3 discontinued treatment early, leaving 66 (sham n = 34, active n = 32) for per-protocol analysis. Depression severity scores reduced in both groups (Montgomery-Asperg Depression Rating Scale reduction in sham = 7.0 [95% CI = 5.0-8.9]; and active = 5.2 [95% CI = 3.2-7.3]). However, there were no differences between active and sham groups in the reduction of depressive symptoms or the number of participants meeting response (sham = 14.7%; active = 3.1%) and remission criteria (sham = 5.9%; active = 0%). Erythema, paresthesia, fatigue, and dizziness/light-headedness occurred more frequently in the active transcranial random noise stimulation group. Neuroplasticity, neuropsychological, and acute cognitive effects were comparable between groups. CONCLUSION: Our results do not support the use of transcranial random noise stimulation with the current stimulation parameters as a therapeutic intervention for the treatment of depression. CLINICAL TRIAL REGISTRATION AT CLINICALTRIALS: gov/NCT01792414.