Alcohol septal ablation for left ventricular outflow tract obstruction in cardiac amyloidosis: New indication for an established therapy.

Cardiac amyloidosis can occasionally demonstrate an atypical pattern of infiltration, causing asymmetric septal thickening and a left ventricular outflow tract (LVOT) gradient with systolic anterior motion (SAM) of the mitral valve resembling obstructive hypertrophic cardiomyopathy. We present a case of a 70-year-old man with cardiac light-chain amyloidosis and LVOT obstruction successfully treated with alcohol septal ablation (ASA). Following the procedure, he reported significant improvement in his heart failure symptoms as well as improvement in LVOT gradient and SAM of the mitral valve. This case demonstrates that ASA is a technically feasible and effective procedure for relieving LVOT obstruction in cardiac amyloidosis and can be considered as a treatment option in patients whose symptoms are refractory to medical therapy.

Coronary artery disease and revascularization associated with immune checkpoint blocker myocarditis: Report from an international registry.

PURPOSE: Immune checkpoint blocker (ICB) associated myocarditis (ICB-myocarditis) may present similarly and/or overlap with other cardiac pathology including acute coronary syndrome presenting a challenge for prompt clinical diagnosis. METHODS: An international registry was used to retrospectively identify cases of ICB-myocarditis. Presence of coronary artery disease (CAD) was defined as coronary artery stenosis >70% in patients undergoing coronary angiogram. RESULTS: Among 261 patients with clinically suspected ICB-myocarditis who underwent a coronary angiography, CAD was present in 59/261 patients (22.6%). Coronary revascularization was performed during the index hospitalisation in 19/59 (32.2%) patients. Patients undergoing coronary revascularization less frequently received steroids administration within 24 h of admission compared to the other groups (p = 0.029). Myocarditis-related 90-day mortality was 9/17 (52.7%) in the revascularised cohort, compared to 5/31 (16.1%) in those not revascularized and 25/156 (16.0%) in those without CAD (p = 0.001). Immune-related adverse event-related 90-day mortality was 9/17 (52.7%) in the revascularized cohort, compared to 6/31 (19.4%) in those not revascularized and 31/156 (19.9%) in no CAD groups (p = 0.007). All-cause 90-day mortality was 11/17 (64.7%) in the revascularized cohort, compared to 13/31 (41.9%) in no revascularization and 60/158 (38.0%) in no CAD groups (p = 0.10). After adjustment of age and sex, coronary revascularization remained associated with ICB-myocarditis-related death at 90 days (hazard ratio [HR] = 4.03, 95% confidence interval [CI] 1.84-8.84, p < 0.001) and was marginally associated with all-cause death (HR = 1.88, 95% CI, 0.98-3.61, p = 0.057). CONCLUSION: CAD may exist concomitantly with ICB-myocarditis and may portend a poorer outcome when revascularization is performed. This is potentially mediated through delayed diagnosis and treatment or more severe presentation of ICB-myocarditis.

Technical and clinical study of x-ray-based surface echo probe tracking using an attached fiducial apparatus.

PURPOSE: Several types of structural heart intervention (SHI) use information from multiple imaging modalities to complete an interventional task. For example, in transcatheter aortic valve replacement (TAVR), placement and deployment of a bioprosthetic aortic valve in the aorta is primarily guided by x-ray fluoroscopy (XRF), and echocardiography provides visualization of cardiac anatomy and blood flow. However, simultaneous interpretation of independent x-ray and echo displays remains a challenge for the interventionalist. The purpose of this work was to develop a novel echo/x-ray co-registration solution in which volumetric transthoracic echo (TTE) is transformed to the x-ray coordinate system by tracking the three-dimensional (3D) pose of a probe fiducial attachment from its appearance in two-dimensional (2D) x-ray images. METHODS: A fiducial attachment for a commercial TTE probe consisting of rings of high-contrast ball bearings was designed and fabricated. The 3D pose (position and orientation) of the fiducial attachment is estimated from a 2D x-ray image using an algorithm in which a virtual point cloud model of the attachment is iteratively rotated, translated, and forward-projected onto the image until the average sum-of-squares of grayscale values at the projected points is minimized. Fiducial registration error (FRE) and target registration error (TRE) of this approach were evaluated in phantom studies using TAVR-relevant gantry orientations and four standard acoustic windows for the TTE probe. A patient study was conducted to assess the clinical suitability of the fiducial attachment prototype during TTE imaging of patients undergoing SHI. TTE image quality for the task of guiding a transcatheter procedure was evaluated in a reviewer study. RESULTS: The 3D FRE ranged from 0.32 ± 0.03 mm (mean ± SD) to 1.31 ± 0.05 mm, depending on C-arm orientation and probe acoustic window. The 3D TRE ranged from 1.06 ± 0.03 mm to 2.42 ± 0.06 mm. Fiducial pose estimation was stable when >75% of the fiducial markers were visible in the x-ray image. A panel of reviewers graded the presentation of heart valves in TTE images from 48 SHI patients. While valve presentation did not differ significantly between acoustic windows (P > 0.05), the mitral valve did achieve a significantly higher image quality compared to the aortic and tricuspid valves (P < 0.001). Overall, reviewers perceived sufficient image quality in 76.5% of images of the mitral valve, 54.9% of images of the aortic valve, and 48.6% of images of the tricuspid valve. CONCLUSIONS: Fiducial-based tracking of a commercial TTE probe is compatible with clinical SHI workflows and yields 3D target registration error of less than 2.5 mm for a variety of x-ray gantry geometries and echo probe acoustic windows. Although TTE image quality with respect to target valve anatomy was sufficient for the majority of cases examined, prescreening of patients for sufficient TTE quality would be helpful.

Cardiotoxicity of anticancer treatments.

Patients with cancer can experience adverse cardiovascular events secondary to the malignant process itself or its treatment. Patients with cancer might also have underlying cardiovascular illness, the consequences of which are often exacerbated by the stress of the tumour growth or its treatment. With the advent of new treatments and subsequent prolonged survival time, late effects of cancer treatment can become clinically evident decades after completion of therapy. The heart's extensive energy reserve and its ability to compensate for reduced function add to the complexity of diagnosis and timely initiation of therapy. Additionally, modern oncological treatment regimens often incorporate multiple agents whose deleterious cardiac effects might be additive or synergistic. Treatment-related impairment of cardiac contractility can be either transient or irreversible. Furthermore, cancer treatment is associated with life-threatening arrhythmia, ischaemia, infarction, and damage to cardiac valves, the conduction system, or the pericardium. Awareness of these processes has gained prominence with the arrival of strategies to monitor and to prevent or to mitigate the effects of cardiovascular damage. A greater understanding of the mechanisms of injury can prolong the lives of those cured of their malignancy, but left with potentially devastating cardiac sequelae.

Enigmas regarding the true extent and impact of tyrosine kinase inhibitor-related cardiotoxicity.

Cardiac sequelae of anticancer treatment remains a major concern among both oncologists and cardiologists caring for patients treated with potentially cardiotoxic regimens. While the toxicity of anthracyclines is well understood to destroy myocytes, the scenario with regard to newer agents, both monoclonal antibodies and small-molecule tyrosine kinase inhibitors, is substantially different. This article differentiates the toxicity of agents that directly destroy myocytes (type I agents) from those that are associated with cardiac damage more indirectly (type II agents). Some mechanistic considerations regarding type II toxicity, albeit not categorically proven, are presented.

Cardiotoxicity of anticancer treatments: what the cardiologist needs to know.

Cardiotoxicity of anticancer treatments has become an increasingly important clinical problem faced by cardiologists. Left ventricular systolic dysfunction and heart failure generate the most concern, but clinical features and prognosis vary considerably depending on the causative agent. Anthracycline-related cardiomyopathy differs fundamentally from effects associated with newer targeted agents, such as trastuzumab. Other forms of cardiovascular disease that occur as a result of cancer treatment include hypertension, thromboembolic disease, pericardial disease, arrhythmia, and myocardial ischemia. The approach to cardiovascular disease in patients with cancer is often different from that in the general population, not only because of distinct underlying mechanisms and clinical features of their heart disease, but also because of the potential ongoing need for additional cancer treatment as well as the altered duration of anticipated survival. In an effort to maximize both quality of life and survival, cardiologists and oncologists should collaborate with the aim of balancing the risks of cardiotoxicity with the benefits of oncologic therapy.

Cardiotoxicity profile of trastuzumab.

Trastuzumab is a monoclonal antibody that targets the human epidermal growth factor receptor tyrosine kinase HER2/ErbB2. This agent has shown a highly significant antitumour effect for patients with HER2-positive breast cancer, and is now considered part of the standard regimens for the treatment of this disease in both the metastatic and adjuvant setting. Cardiotoxicity has been associated with trastuzumab, and this issue has now been studied and documented in a number of adjuvant trials for which data have now been released. Cardiotoxicity has been shown to be potentiated when the agent is used concurrently or sequentially with an anthracycline, and this has limited the use of trastuzumab in some patients. Determining the overall impact of trastuzumab is further complicated by the administration of other cardiotoxic agents such as the taxanes and cyclophosphamide as well as by pre-existing cardiac disease. The incidence of severe congestive heart failure (New York Heart Association class III or IV) was 0-3.9% in the trastuzumab arms versus 0-1.3% in the control arms in the five major randomized adjuvant trials. Only one cardiac death was related to trastuzumab whereas two cardiac deaths occurred in the control arms. Ejection fraction decline of >or=10% or 15% was reported in 3-34% of trastuzumab recipients in these trials. Patients affected by trastuzumab-related cardiotoxicity do not exhibit the cellular death and distinctive ultrastructural myocardial changes seen on electron microscopy with anthracycline-induced cardiotoxicity. The cardiotoxicity of trastuzumab also differs from traditional chemotherapy-induced cardiotoxicity in that it appears to be at least partially reversible, not related to the cumulative dose, and re-challenge is generally tolerated. There remain a number of uncertainties regarding the diagnosis and management of trastuzumab-related cardiotoxicity. While no formal guidelines or consensus statements exist at present regarding cardiac monitoring during use of trastuzumab, proposed recommendations include a careful assessment of ejection fraction prior to initiating trastuzumab, avoidance of concurrent administration of trastuzumab with anthracyclines, and regular monitoring of symptoms and cardiac function during and for several years after therapy. Increased vigilance is appropriate for higher risk patients.