Diagnostic performance of quantitative coronary artery disease assessment using computed tomography in patients with aortic stenosis undergoing transcatheter aortic-valve implantation.

BACKGROUND: Computed tomography angiography (CTA) is a cornerstone in the pre- transcatheter aortic valve replacement (TAVI) assessment. We evaluated the diagnostic performance of CTA and coronary artery calcium score (CACS) for CAD evaluation compared to invasive coronary angiography in a cohort of TAVI patients. METHODS: In consecutive TAVI patients without prior coronary revascularization and device implants, CAD was assessment by quantitative analysis in CTA. (a) Patients with non-evaluable segments were classified as obstructive CAD. (b) In patients with non-evaluable segments a CACS cut-off of 100 was applied for obstructive CAD. The reference standard was quantitative invasive coronary angiography (QCA, i.e. ≥ 50% stenosis). RESULTS: 100 consecutive patients were retrospectively included, age was 82.3 ± 6.5 years and 30% of patients had CAD. In 16% of the patients, adequate visualization of the entire coronary tree (all 16 segments) was possible with CTA, while 84% had at least one segment which was not evaluable for CAD analysis due to impaired image quality. On a per-patient analysis, where patients with low image quality were classified as CAD, CTA showed a sensitivity of 100% (95% CI 88.4-100.0), specificity of 11.4% (95% CI 5.1-21.3), PPV of 32.6% (95% CI 30.8-34.5), NPV of 100% and diagnostic accuracy of 38% (95% CI 28.5-48.3) for obstructive CAD. When applying a combined approach of CTA (in patients with good image quality) and CACS (in patients with low image quality), the sensitivity and NPV remained at 100% and obstructive CAD could be ruled out in 20% of the TAVI patients, versus 8% using CTA alone. CONCLUSION: In routinely acquired pre-TAVI CTA, the image quality was insufficient in a high proportion of patients for the assessment of the entire coronary artery tree. However, when adding CACS in patients with low image quality to quantitative CTA assessment in patients with good image quality, obstructive CAD could be ruled-out in 1/5 of the patients and may therefore constitute a strategy to streamline pre-procedural workup, and reduce risk, radiation and costs in selected TAVI patients without prior coronary revascularization or device implants.

Systemic Corticosteroid Exposure and Atrioventricular Conductance Delays After Transcatheter Aortic Valve Implantation.

BACKGROUND: Atrioventricular conduction delays (AVCD) are common after transcatheter aortic valve implantation (TAVI) and frequently require implantation of a permanent pacemaker (PPM). Autopsy studies demonstrated the role of ischemia, inflammation, and oedema in the pathogenesis of AVCD. Corticosteroids (CS) reduce inflammation and oedema and hence might lead to a lower rate of AVCD. METHODS: Based on a prospective single-center registry, we performed a propensity score (PS) matched analysis of subjects treated with or without systemic CS (>2.5 mg prednisolone-equivalent per day) at the time of TAVI. The primary endpoint was a composite of PPM-implantation and new-onset left bundle branch block (LBBB) within 30 days after TAVI. RESULTS: Among 2213 consecutive patients undergoing TAVI (51.5% female, mean age 82.1 ± 6.1 years) 89 patients were treated with systemic CS, of which 87 were included in the PS matched analysis. At 30 days, rates of the composite of PPM and LBBB were comparable between patients with versus without CS both in the overall cohort (33.7% versus 33.0%, p = 0.89) and the PS matched cohort (34.5% versus 40.2%, p = 0.443). There were no differences in a composite of major or minor vascular complications and major or life-threatening bleeding events between patients with versus without CS in the overall cohort (34.8% versus 26.6%, p = 0.088) or the PS matched cohort (33.3% versus 33.3%, p ≥ 0.999). CONCLUSION: In this exploratory study, intake of systemic CS among patients undergoing TAVI was not associated with differences in rates of AVCD, vascular complications, or bleeding events after TAVI.

Shockwave Intravascular Lithotripsy of Calcified Coronary Lesions in ST-Elevation Myocardial Infarction: First-in-Man Experience.

We present the first cases of Shockwave intravascular lithotripsy (S-IVL; Shockwave Medical), a novel coronary calcium modification device, being used in patients undergoing percutaneous coronary intervention for ST-elevation myocardial infarction (STEMI). The 3 presented cases include an upfront use of S-IVL in a right coronary artery, an in-stent restenosis, and a community cardiac arrest/STEMI equivalent where S-IVL was used as a bail-out technique to facilitate stent delivery in a tortuous calcified vessel.

Treatment of Heavily Calcified Unprotected Left Main Disease With Lithotripsy: The First Case Series.

We present the first case series using Shockwave Intravascular Lithotripsy (S-IVL; Shockwave Medical), a novel coronary calcium modification device, in patients with heavily calcified unprotected left main (LM) coronary artery disease (CAD). Decisions regarding surgical vs percutaneous revascularization in LM-CAD patients are based on anatomical complexity and perceived surgical risk. In this series, we present the use of S-IVL in a patient with LM-CAD with multivessel disease who declined surgery, a patient with an isolated LM-CAD and severe cardiomyopathy, and a late nonagenarian patient where surgical revascularization was not an option.

A systematic review of clozapine-induced myocarditis.

BACKGROUND: Clozapine is an atypical antipsychotic that is beneficial to some patients who failed to have an adequate clinical response to other antipsychotic drugs. Its clinical use is limited due to several potentially fatal adverse reactions including myocarditis. Careful monitoring of patients on clozapine is required. METHODS: We conducted a systematic review of the literature on myocarditis associated with clozapine therapy. The search engines used to identify cases were MEDLINE, EMBASE, PsycINFO and Cochrane reviews. The references included in the manuscripts reviewed were searched to identify additional reports. RESULTS: We identified a total of 3347 articles that addressed the cardiac complications of clozapine. Of these, 82 articles detailed cases of clozapine-induced myocarditis. The median age of patients and dose of clozapine at presentation was 30years and 250mg/day respectively. Symptoms and signs of myocarditis developed in 87% of patients within the first month of treatment. Clinical presentation included: shortness of breath (67%), fever (67%) and tachycardia (58%). Cardiac markers were elevated in 87% of the 54 cases that reported these markers. Global ventricular dysfunction was the predominant echocardiogram finding (57%). CONCLUSIONS: Patients on clozapine require routine monitoring for symptoms and signs of myocarditis during the first three months of therapy. This adverse drug reaction is difficult to diagnose due the non-specific nature of the symptoms and signs. Alternate causes of myocarditis should be ruled out before attributing the myocarditis to clozapine.

A systematic review of clozapine induced cardiomyopathy.

BACKGROUND: Clozapine is a unique anti-psychotic medication that is most effective in the treatment of refractory schizophrenia and reducing suicidality. Cardiomyopathy is among the side effects of this medication that limits its use. There are a number of case reports, case series and expert opinion papers discussing clozapine induced cardiomyopathy, but there is no evidence-based review of the subject to guide clinicians. METHODS: We undertook a systematic review of the literature on cardiomyopathy associated with clozapine. The primary systemic search was in MEDLINE but EMBASE, PsycINFO, and Cochrane were searched and manufacturers of clozapine were contacted for cases. Articles were then individually reviewed to find additional reports. RESULTS: We identified 17 articles detailing 26 individual cases and 11 additional articles without individual case data. The mean age at time of diagnosis was 33.5 years. The mean dose of clozapine on presentation was 360 mg. Symptoms developed at an average of 14.4 months after initiating clozapine. The clinical presentation was generally consistent with heart failure: including shortness of breath (60%) and palpitations (36%). Echocardiography at presentation showed dilated cardiomyopathy in 39% of cases and was not specified in other cases. CONCLUSION: There should be a low threshold in performing echocardiography in suspected cases of clozapine induced cardiomyopathy. Clozapine should be withheld in the setting of cardiomyopathy without other explanation. There is limited data on the safety of drug re-challenge in clozapine induced cardiomyopathy. Re-challenge may be considered in carefully selected cases but close monitoring and frequent echocardiography are required.