Pacemaker malfunction risks within the electromagnetically rich hospital environment

We encourage the readers to exercise increased awareness, perform detailed risk-benefit assessments, and apply risk mitigation strategies for patients with implantable devices who may be exposed to hostile electromagnetic hospital environments

Use of orbital atherectomy in acute myocardial infarction via the transradial approach

Severe coronary artery calcifications pose an ongoing challenge when performing percutaneous coronary interventions, resulting in an increased likelihood of procedural complications. Orbital atherectomy (OA) has emerged as a promising technology that helps improve outcomes in this complex patient population. Its safety and efficacy are yet to be demonstrated in the setting of acute myocardial infarction. We present a case of a patient with acute ST-elevation myocardial infarction (STEMI) evaluated with emergent transradial coronary angiography. The culprit lesion was a severely stenotic, heavily calcified, segment of the right coronary artery. The use of OA facilitated lesion expansion and implantation of a drug-eluting stent. Although OA should be considered as contraindicated for the management of soft-ruptured plaque, which accounts for the majority of STEMI presentations, it may be well applied to the small subset of patients with calcified nodule pathology, even in the acute setting

Triple-Vessel Percutaneous Coronary Revascularization In Situs Inversus Dextrocardia

Dextrocardia with situs inversus occurs in approximately one in 10,000 individuals of whom 20% have primary ciliary dyskinesia inherited as an autosomal recessive trait. These patients have a high incidence of congenital cardiac disease but their risk of coronary artery disease is similar to that of the general population. We report what is, to our knowledge, the first case of total triple-vessel coronary revascularization by percutaneous stent implantation in a 79-year-old woman with situs inversus dextrocardia. We describe the successful use of standard diagnostic and interventional guide catheters with counter rotation and transversely inversed image acquisition techniques. The case also highlights that the right precordial pain may represent cardiac ischemia in this population

Risk Factors for Nonplatelet Thromboxane Generation After Coronary Artery Bypass Graft Surgery

BACKGROUND: Persistent thromboxane (TX) generation while receiving aspirin therapy is associated with an increased risk of cardiovascular events. The Reduction in Graft Occlusion Rates (RIGOR) study found that aspirin-insensitive TXA2 generation, indicated by elevated urine 11-dehydro-TXB2 (UTXB2) 6 months after coronary artery bypass graft surgery, was a potent risk factor for vein graft thrombosis and originated predominantly from nonplatelet sources. Our goal was to identify risks factors for nonplatelet TXA2 generation. METHODS AND RESULTS: Multivariable modeling was performed by using clinical and laboratory variables obtained from 260 RIGOR subjects with verified aspirin-mediated inhibition of platelet TXA2 generation. The strongest variable associated with UTXB2 6 months after surgery, accounting for 47.2% of the modeled effect, was urine 8-iso-prostaglandin (PG)F2alpha, an arachidonic acid metabolite generated nonenzymatically by oxidative stress (standardized coefficient 0.442, P \u3c 0.001). Age, sex, race, lipid therapy, creatinine, left ventricular ejection fraction, and aspirin dose were also significantly associated with UTXB2 (P \u3c 0.03), although they accounted for only 4.8% to 10.2% of the modeled effect. Urine 8-iso-PGF2alpha correlated with risk of vein graft occlusion (odds ratio 1.67, P=0.001) but was not independent of UTXB2. In vitro studies revealed that endothelial cells generate TXA2 in response to oxidative stress and direct exposure to 8-iso-PGF2alpha. CONCLUSIONS: Oxidative stress-induced formation of 8-iso-PGF2alpha is strongly associated with nonplatelet thromboxane formation and early vein graft thrombosis after coronary artery bypass graft surgery. The endothelium is potentially an important source of oxidative stress-induced thromboxane generation. These findings suggest therapies that reduce oxidative stress could be useful in reducing cardiovascular risks associated with aspirin-insensitive thromboxane generation

The Double Loaded LV: High Prevalence of Hypertensive LVH Preceding the Development of Severe Aortic Stenosis

Background: It is generally assumed that left ventricular hypertrophy (LVH) in aortic stenosis (AS) is a compensatory adaptation to chronic outflow obstruction. However the advent of TAVR has stimulated more focus on AS in older patients, most of whom have antecedent hypertension (HTN). Accordingly our aim was to investigate the interaction between HTN and AS on LV remodeling in contemporary practice. Methods: We studied 33 consecutive patients with AV peak velocity (PV) \u3e2.5 m/s on their initial echo and a PV of \u3e3.5 m/s on a subsequent study performed at least 5 years later. Patients’ demographics and clinical information were collected. Peak intraventricular pressure (IVP, mmHg) was defined as the sum of systolic arterial pressure and peak intraventricular gradient.Data were analyzed using descriptive statistics, paired- samples T test, and linear correlation. Results: Of our sample (46% women, mean age of 82±11 y), 29 (88%) had a history of hypertension. The average interval between the two echo studies was 6.2±1 years. As expected, wall thickness, LV Mass, and relative wall thickness increased over time. There was no correlation between change in LV mass index (LVMi, g/m2) and peak IVP, PV or AV MG. However change in LVMi did correlate inversely with baseline LVMi (r= -0.37, p= 0.03). Conclusion: Most patients seen in our practice with severe AS have antecedent hypertension and LVH. LVH worsens in parallel with worsening severity of AS. Remodeling in these patients features increasing concentric remodeling of the LV, rather than LV dilation. Given these findings, we speculate that regression of LVH to normal will not be effected by AVR because LVH proceeded hemodynamically severe AS. Strict control of blood pressure might be of equal importance in preventing and ameliorating pressure overload in these patients

Percutaneous Valvuloplasty for Bioprosthetic Tricuspid Valve Stenosis

Percutaneous transcatheter tricuspid balloon valvuloplasty (PTTBV) is an accepted treatment option for symptomatic severe native tricuspid valve stenosis, although surgical tricuspid valve replacement remains the treatment of choice. There have been few reports of successful PTTBV for bioprosthetic tricuspid valve stenosis. We present case reports of 3 patients from our hospital experience. Two of the 3 cases were successful, with lasting clinical improvement, whereas the 3rd patient failed to show a reduction in valve gradient. We describe the standard technique used for PTTBV. We present results from a literature review that identified 16 previously reported cases of PTTBV for bioprosthetic severe tricuspid stenosis, with overall favorable results. We conclude that PTTBV should perhaps be considered for a select patient population in which symptomatic improvement and hemodynamic stability are desired immediately, and particularly for patients who are inoperable or at high surgical risk

Differentiating Pseudo Versus True Aortic Stenosis in Patients Without Contractile Reserve: A Diagnostic Dilemma

Low-flow, low-gradient (LF-LG) aortic stenosis with depressed left ventricular (LV) ejection fraction is a diagnostic challenge that is frequently encountered in the management of valvular heart disease. True-severe LF-LG aortic stenosis is amenable to valve replacement, whereas pseudo-severe aortic stenosis requires management of the underlying cardiomyopathy. This distinction is important as it serves as a critical branch point in guiding therapeutic decisions. We present the case of a 71-year-old male with LF-LG aortic stenosis who had a reduced and biphasic augmentation of LV flow during dobutamine stress echocardiography (DSE). Further evaluation revealed a stenotic left subclavian artery proximal to the left internal mammary artery graft to the left anterior descending (LAD) artery. Bypass of the subclavian stenosis reversed the LAD territory ischemia and confirmed pseudo-severe aortic stenosis on repeat DSE. Traditional DSE parameters are inconclusive in patients with LF-LG aortic stenosis with poor flow reserve. Calculation of the projected orifice area or measurement of aortic valve calcium via multidetector computed tomography (MDCT) may be required in this scenario. Most importantly, reversible causes of LV dysfunction identified during DSE for LF-LG aortic stenosis require a different treatment approach than that of true aortic stenosis

Differential Impact of Serial Measurement of Nonplatelet Thromboxane Generation on Long-Term Outcome After Cardiac Surgery.

BACKGROUND: Systemic thromboxane generation, not suppressible by standard aspirin therapy and likely arising from nonplatelet sources, increases the risk of atherothrombosis and death in patients with cardiovascular disease. In the RIGOR (Reduction in Graft Occlusion Rates) study, greater nonplatelet thromboxane generation occurred early compared with late after coronary artery bypass graft surgery, although only the latter correlated with graft failure. We hypothesize that a similar differential association exists between nonplatelet thromboxane generation and long-term clinical outcome. METHODS AND RESULTS: Five-year outcome data were analyzed for 290 RIGOR subjects taking aspirin with suppressed platelet thromboxane generation. Multivariable modeling was performed to define the relative predictive value of the urine thromboxane metabolite, 11-dehydrothromboxane B CONCLUSIONS: Long-term nonplatelet thromboxane generation after coronary artery bypass graft surgery is a novel risk factor for 5-year adverse outcome, including death. In contrast, nonplatelet thromboxane generation in the early postoperative period appears to be driven predominantly by inflammation and did not independently predict long-term clinical outcome

Inhibition of transforming growth factor-β restores endothelial thromboresistance in vein grafts

BackgroundThrombosis is a major cause of the early failure of vein grafts (VGs) implanted during peripheral and coronary arterial bypass surgeries. Endothelial expression of thrombomodulin (TM), a key constituent of the protein C anticoagulant pathway, is markedly suppressed in VGs after implantation and contributes to local thrombus formation. While stretch-induced paracrine release of transforming growth factor-β (TGF-β) is known to negatively regulate TM expression in heart tissue, its role in regulating TM expression in VGs remains unknown.MethodsChanges in relative mRNA expression of major TGF-β isoforms were measured by quantitative polymerase chain reaction (qPCR) in cultured human saphenous vein smooth muscle cells (HSVSMCs) subjected to cyclic stretch. To determine the effects of paracrine release of TGF-β on endothelial TM mRNA expression, human saphenous vein endothelial cells (HSVECs) were co-cultured with stretched HSVSMCs in the presence of 1D11, a pan-neutralizing TGF-β antibody, or 13C4, an isotype-control antibody. Groups of rabbits were then administered 1D11 or 13C4 and underwent interpositional grafting of jugular vein segments into the carotid circulation. The effect of TGF-β inhibition on TM gene expression was measured by qPCR; protein C activating capacity and local thrombus formation were measured by in situ chromogenic substrate assays; and VG remodeling was assessed by digital morphometry.ResultsCyclic stretch induced TGF-β1 expression in HSVSMCs by 1.9 ± 0.2-fold (P < .001) without significant change in the expressions of TGF-β2 and TGF-β3. Paracrine release of TGF-β1 by stretched HSVSMCs inhibited TM expression in stationary HSVECs placed in co-culture by 57 ± 12% (P = .03), an effect that was abolished in the presence of 1D11. Similarly, TGF-β1 was the predominant isoform induced in rabbit VGs 7 days after implantation (3.5 ± 0.4-fold induction; P < .001). TGF-β1 protein expression localized predominantly to the developing neointima and coincided with marked suppression of endothelial TM expression (16% ± 2% of vein controls; P < .03), a reduction in situ activated protein C (APC)-generating capacity (53% ± 9% of vein controls; P = .001) and increased local thrombus formation (3.7 ± 0.8-fold increase over vein controls; P < .01). External stenting of VGs to limit vessel distension significantly reduced TGF-β1 induction and TM downregulation. Systemic administration of 1D11 also effectively prevented TM downregulation, preserved APC-generating capacity, and reduced local thrombus in rabbit VGs without observable effect on neointima formation and other morphometric parameters 6 weeks after implantation.ConclusionTM downregulation in VGs is mediated by paracrine release of TGF-β1 caused by pressure-induced vessel stretch. Systemic administration of an anti-TGF-β antibody effectively prevented TM downregulation and preserved local thromboresistance without negative effect on VG remodeling.Clinical RelevanceVein grafts (VGs) are commonly used conduits for coronary and peripheral arterial bypass surgeries. Thrombosis is a major cause of early VG failure. Trombomodulin (TM), a key component of the anticoagulant protein C pathway, is downregulated early after VG implantation and facilitates local thrombus formation. We found that paracrine release of transforming growth factor-β1 (TGF-β1), caused by pressure-induced stretch, was a potent negative regulator of TM in rabbit VGs. Administration of a neutralizing anti-TGF-β antibody effectively prevented TM downregulation and reduced local thrombus generation without adversely affecting long-term VG remodeling. This may represent a novel strategy to improve patency in patients undergoing arterial bypass procedures

Rationale and design of SAVI-AoS:A physiologic study of patients with symptomatic moderate aortic valve stenosis and preserved left ventricular ejection fraction

Background: Moderate aortic valve stenosis occurs twice as often as severe aortic stenosis (AS) and carries a similarly poor prognosis. Current European and American guidelines offer limited insight into moderate AS (MAS) patients with unexplained symptoms. Measuring valve physiology at rest while most patients experience symptoms during exertion might represent a conceptual limitation in the current grading of AS severity. The stress aortic valve index (SAVI) may delineate hemodynamically significant AS among patients with MAS. Objectives: To investigate the diagnostic value of SAVI in symptomatic MAS patients with normal left ventricular ejection fraction (LVEF ≥ 50%): aortic valve area (AVA) > 1 cm2 plus either mean valve gradient (MG) 15–39 mmHg or maximal aortic valve velocity (AOV max) 2.5–3.9 m/s. Short-term objectives include associations with symptom burden, functional capacity, and cardiac biomarkers. Long-term objectives include clinical outcomes. Methods and results: Multicenter, non-blinded, observational cohort. AS severity will be graded invasively (aortic valve pressure measurements with dobutamine stress testing for SAVI) and non-invasively (echocardiography during dobutamine and exercise stress). Computed tomography (CT) of the aortic valve will be scored for calcium, and hemodynamics simulated using computational fluid dynamics. Cardiac biomarkers and functional parameters will be serially monitored. The primary objective is to see how SAVI and conventional measures (MG, AVA and Vmax) correlate with clinical parameters (quality of life survey, 6-minute walk test [6MWT], and biomarkers). Conclusions: The SAVI-AoS study will extensively evaluate patients with unexplained, symptomatic MAS to determine any added value of SAVI versus traditional, resting valve parameters