Transthoracic delivery of large devices into the left ventricle through the right ventricle and interventricular septum: preclinical feasibility.

BACKGROUND: We aim to deliver large appliances into the left ventricle through the right ventricle and across the interventricular septum. This transthoracic access route exploits immediate recoil of the septum, and lower transmyocardial pressure gradient across the right versus left ventricular free wall. The route may enhance safety and allow subxiphoid rather than intercostal traversal. METHODS: The entire procedure was performed under real-time CMR guidance. An "active" CMR needle crossed the chest, right ventricular free wall, and then the interventricular septum to deliver a guidewire then used to deliver an 18Fr introducer. Afterwards, the right ventricular free wall was closed with a nitinol occluder. Immediate closure and late healing of the unrepaired septum and free wall were assessed by oximetry, angiography, CMR, and necropsy up to four weeks afterwards. RESULTS: The procedure was successful in 9 of 11 pigs. One failed because of refractory ventricular fibrillation upon needle entry, and the other because of inadequate guidewire support. In all ten attempts, the right ventricular free wall was closed without hemopericardium. There was neither immediate nor late shunt on oximetry, X-ray angiography, or CMR. The interventricular septal tract fibrosed completely. Transventricular trajectories planned on human CT scans suggest comparable intracavitary working space and less acute entry angles than a conventional atrial transseptal approach. CONCLUSION: Large closed-chest access ports can be introduced across the right ventricular free wall and interventricular septum into the left ventricle. The septum recoils immediately and heals completely without repair. A nitinol occluder immediately seals the right ventricular wall. The entry angle is more favorable to introduce, for example, prosthetic mitral valves than a conventional atrial transseptal approach.

Extracellular volume fraction mapping in the myocardium, part 1: evaluation of an automated method.

BACKGROUND: Disturbances in the myocardial extracellular volume fraction (ECV), such as diffuse or focal myocardial fibrosis or edema, are hallmarks of heart disease. Diffuse ECV changes are difficult to assess or quantify with cardiovascular magnetic resonance (CMR) using conventional late gadolinium enhancement (LGE), or pre- or post-contrast T1-mapping alone. ECV measurement circumvents factors that confound T1-weighted images or T1-maps, and has been shown to correlate well with diffuse myocardial fibrosis. The goal of this study was to develop and evaluate an automated method for producing a pixel-wise map of ECV that would be adequately robust for clinical work flow. METHODS: ECV maps were automatically generated from T1-maps acquired pre- and post-contrast calibrated by blood hematocrit. The algorithm incorporates correction of respiratory motion that occurs due to insufficient breath-holding and due to misregistration between breath-holds, as well as automated identification of the blood pool. Images were visually scored on a 5-point scale from non-diagnostic (1) to excellent (5). RESULTS: The quality score of ECV maps was 4.23 ± 0.83 (m ± SD), scored for n=600 maps from 338 patients with 83% either excellent or good. Co-registration of the pre-and post-contrast images improved the image quality for ECV maps in 81% of the cases. ECV of normal myocardium was 25.4 ± 2.5% (m ± SD) using motion correction and co-registration values and was 31.5 ± 8.7% without motion correction and co-registration. CONCLUSIONS: Fully automated motion correction and co-registration of breath-holds significantly improve the quality of ECV maps, thus making the generation of ECV-maps feasible for clinical work flow.

Extracellular volume fraction mapping in the myocardium, part 2: initial clinical experience.

BACKGROUND: Diffuse myocardial fibrosis, and to a lesser extent global myocardial edema, are important processes in heart disease which are difficult to assess or quantify with cardiovascular magnetic resonance (CMR) using conventional late gadolinium enhancement (LGE) or T1-mapping. Measurement of the myocardial extracellular volume fraction (ECV) circumvents factors that confound T1-weighted images or T1-maps. We hypothesized that quantitative assessment of myocardial ECV would be clinically useful for detecting both focal and diffuse myocardial abnormalities in a variety of common and uncommon heart diseases. METHODS: A total of 156 subjects were imaged including 62 with normal findings, 33 patients with chronic myocardial infarction (MI), 33 with hypertrophic cardiomyopathy (HCM), 15 with non-ischemic dilated cardiomyopathy (DCM), 7 with acute myocarditis, 4 with cardiac amyloidosis, and 2 with systemic capillary leak syndrome (SCLS). Motion corrected ECV maps were generated automatically from T1-maps acquired pre- and post-contrast calibrated by blood hematocrit. Abnormally-elevated ECV was defined as >2SD from the mean ECV in individuals with normal findings. In HCM the size of regions of LGE was quantified as the region >2 SD from remote. RESULTS: Mean ECV of 62 normal individuals was 25.4 ± 2.5% (m ± SD), normal range 20.4%-30.4%. Mean ECV within the core of chronic myocardial infarctions (without MVO) (N=33) measured 68.5 ± 8.6% (p<0.001 vs normal). In HCM, the extent of abnormally elevated ECV correlated to the extent of LGE (r=0.72, p<0.001) but had a systematically greater extent by ECV (mean difference 19 ± 7% of slice). Abnormally elevated ECV was identified in 4 of 16 patients with non-ischemic DCM (38.1 ± 1.9% (p<0.001 vs normal) and LGE in the same slice appeared "normal" in 2 of these 4 patients. Mean ECV values in other disease entities ranged 32-60% for cardiac amyloidosis (N=4), 40-41% for systemic capillary leak syndrome (N=2), and 39-56% within abnormal regions affected by myocarditis (N=7). CONCLUSIONS: ECV mapping appears promising to complement LGE imaging in cases of more homogenously diffuse disease. The ability to display ECV maps in units that are physiologically intuitive and may be interpreted on an absolute scale offers the potential for detection of diffuse disease and measurement of the extent and severity of abnormal regions.

MultiContrast Delayed Enhancement (MCODE) improves detection of subendocardial myocardial infarction by late gadolinium enhancement cardiovascular magnetic resonance: a clinical validation study.

BACKGROUND: Myocardial infarction (MI) documented by late gadolinium enhancement (LGE) has clinical and prognostic importance, but its detection is sometimes compromised by poor contrast between blood and MI. MultiContrast Delayed Enhancement (MCODE) is a technique that helps discriminate subendocardial MI from blood pool by simultaneously providing a T2-weighted image with a PSIR (phase sensitive inversion recovery) LGE image. In this clinical validation study, our goal was to prospectively compare standard LGE imaging to MCODE in the detection of MI. METHODS: Imaging was performed on a 1.5 T scanner on patients referred for CMR including a LGE study. Prospective comparisons between MCODE and standard PSIR LGE imaging were done by targeted, repeat imaging of slice locations. Clinical data were used to determine MI status. Images at each of multiple time points were read on separate days and categorized as to whether or not MI was present and whether an infarction was transmural or subendocardial. The extent of infarction was scored on a sector-by-sector basis. RESULTS: Seventy-three patients were imaged with the specified protocol. The majority were referred for vasodilator perfusion exams and viability assessment (37 ischemia assessment, 12 acute MI, 10 chronic MI, 12 other diagnoses). Forty-six patients had a final diagnosis of MI (30 subendocardial and 16 transmural). MCODE had similar specificity compared to LGE at all time points but demonstrated better sensitivity compared to LGE performed early and immediately before and after the MCODE (p = 0.008 and 0.02 respectively). Conventional LGE only missed cases of subendocardial MI. Both LGE and MCODE identified all transmural MI. Based on clinical determination of MI, MCODE had three false positive MI's; LGE had two false positive MI's including two of the three MCODE false positives. On a per sector basis, MCODE identified more infarcted sectors compared to LGE performed immediately prior to MCODE (p < 0.001). CONCLUSION: While both PSIR LGE and MCODE were good in identifying MI, MCODE demonstrated more subendocardial MI's than LGE and identified a larger number of infarcted sectors. The simultaneous acquisition of T1 and T2-weighted images improved differentiation of blood pool from enhanced subendocardial MI.

The Association of Erectile Dysfunction and Cardiovascular Disease: A Systematic Critical Review.

Despite strong association between erectile dysfunction (ED) and cardiovascular disease (CVD), there is a paucity of clear clinical guidelines detailing when and how to evaluate for ED in patients with known CVD, or vice versa. This systematic review discuss the role of cardiologists and urologists in the characterization of risk and management of CVD in the setting of ED, as well as contrasting the current evaluation of CVD and ED from the standpoint of published consensus statements. A comprehensive literature review utilizing MEDLINE®, the Cochrane Library® Central Search, and the Web of Science was performed to identify all published peer-reviewed articles in the English language describing ED and CVD across various disciplines. There is strong consensus that men with ED should be considered at high risk of CVD. Available risk assessment tools should be used to stratify the coronary risk score in each patient. The 2012 Princeton III Consensus Conference expanded on existing cardiovascular recommendations, proposing an approach to the evaluation and management of cardiovascular risk in men with ED and no known CVD. This systematic review highlights the similarities and differences of the existing clinical guidelines and recommendations regarding assessment and management of ED and CVD, as well as the pathophysiological linkage between ED and CVD, which may permit physicians, including urologists, to perform opportunistic screening and initiate secondary prophylaxis with regard to cardiovascular risk factors, particularly in young, nondiabetic men with ED.

Early Gadolinium Enhancement for Determination of Area at Risk: A Preclinical Validation Study.

OBJECTIVES: The aim of this study was to determine whether early gadolinium enhancement (EGE) by cardiac magnetic resonance (CMR) in a canine model of reperfused myocardial infarction depicts the area at risk (AAR) as determined by microsphere blood flow analysis. BACKGROUND: It remains controversial whether only the irreversibly injured myocardium enhances when CMR is performed in the setting of acute myocardial infarction. Recently, EGE has been proposed as a measure of the AAR in acute myocardial infarction because it correlates well with T2-weighted imaging of the AAR, but this still requires pathological validation. METHODS: Eleven dogs underwent 2 h of coronary artery occlusion and 48 h of reperfusion before imaging at 1.5-T. EGE imaging was performed 3 min after contrast administration with coverage of the entire left ventricle. Late gadolinium enhancement imaging was performed between 10 and 15 min after contrast injection. AAR was defined as myocardium with blood flow <2 SD from remote myocardium determined by microspheres during occlusion. The size of infarction was determined with triphenyltetrazolium chloride. RESULTS: There was no significant difference in the size of enhancement by EGE compared with the size of AAR by microspheres (44.1 ± 15.8% vs. 42.7 ± 9.2%; p = 0.61), with good correlation (r = 0.88; p < 0.001) and good agreement by Bland-Altman analysis (mean bias 1.4 ± 17.4%). There was no difference in the size of enhancement by EGE compared with enhancement on native T1 and T2 maps. The size of EGE was significantly greater than the infarct by triphenyltetrazolium chloride (44.1 ± 15.8% vs. 20.7 ± 14.4%; p < 0.001) and late gadolinium enhancement (44.1 ± 15.8% vs. 23.5 ± 12.7%; p < 0.001). CONCLUSIONS: At 3 min post-contrast, EGE correlated well with the AAR by microspheres and CMR and was greater than infarct size. Thus, EGE enhances both reversibly and irreversibly injured myocardium.

Safety and tolerability of regadenoson CMR.

AIMS: Knowledge of adverse events associated with regadenoson perfusion cardiac magnetic resonance (CMR) and patient tolerability has implications for patient safety and staff training. We sought to assess the safety and tolerability of regadenoson stress CMR. MATERIALS AND METHODS: A group of 728 consecutive patients (median age 58, 44% female) and 25 normal volunteers (median age 21, 24% female) were recruited from August 2009 to March 2012 using a prospective, cross-sectional study design. Subjects were stressed using fixed-dose regadenoson and imaged using a 1.5T MRI scanner. Symptoms and adverse events including death, myocardial infarction (MI), ventricular tachycardia (VT)/ventricular fibrillation (VF), hospitalization, arrhythmias, and haemodynamic stability were assessed. RESULTS: There were no occurrences of death, MI, VT/VF, high-grade atrioventricular block, or stress-induced atrial fibrillation. Notable adverse events included one case of bronchospasm and one case of heart failure exacerbation resulting in hospitalization. The most common symptoms in patients were dyspnoea (30%, n = 217), chest discomfort (27%, n = 200), and headache (15%, n = 111). There was minimal change between baseline and peak systolic and diastolic blood pressure in both patients and volunteers (P > 0.05). A blunted heart rate response to regadenoson was noted in patients with body mass index (BMI) ≥ 30 kg/m(2) (P < 0.001), and diabetes (P = 0.001). CONCLUSIONS: Regadenoson CMR is well tolerated and can be performed safely with few adverse events.

Concordance and diagnostic accuracy of vasodilator stress cardiac MRI and 320-detector row coronary CTA.

Vasodilator stress cardiac magnetic resonance (CMR) detects ischemia whereas coronary CT angiography (CTA) detects atherosclerosis. The purpose of this study was to determine concordance and accuracy of vasodilator stress CMR and coronary CTA in the same subjects. We studied 151 consecutive subjects referred to detect or exclude suspected obstructive coronary artery disease (CAD) in patients without known disease or recurrent stenosis or ischemia in patients with previously treated CAD. Vasodilator stress CMR was performed on a 1.5 T scanner. CTA was performed on a 320-detector row system. Subjects were followed for cardiovascular events and downstream diagnostic testing. Subjects averaged 56 ± 12 years (60% male), and 62 % had intermediate pre-test probability for obstructive CAD. Follow-up averaged 450 ± 115 days and was 100% complete. CMR and CTA agreed in 92% of cases (κ 0.81, p < 0.001). The event-free survival was 97 % for non-ischemic and 39% for ischemic CMR (p < 0.0001). The event-free survival was 99% for non-obstructive and 36% for obstructive CTA (p < 0.0001). Using a reference standard including quantitative invasive angiography or major cardiovascular events, CMR and CTA had respective sensitivities of 93 and 98 %; specificities of 96 and 96%; positive predictive values of 91 and 91%; negative predictive values of 97 and 99%; and accuracies of 95 and 97%. Non-ischemic vasodilator stress CMR or non-obstructive coronary CTA were highly concordant and each confer an excellent prognosis. CMR and CTA are both accurate for assessment of obstructive CAD in a predominantly intermediate risk population.