Noninvasive Multimodality Imaging for the Assessment of Anomalous Coronary Artery.

PURPOSE OF REVIEW: Anomalous aortic origin of a coronary artery (AAOCA) is a rare congenital coronary anomaly with the potential to cause myocardial ischemia and adverse cardiac events. The presence of AAOCA anatomy itself does not necessarily implicate a need for revascularization. Therefore, the purpose of this review is to assess how noninvasive comprehensive anatomic- and physiologic evaluation may guide patient management. RECENT FINDINGS: The assessment of AAOCA includes an accurate description of the anomalous origin/vessel course including anatomical high-risk features such as a slit-like ostium, proximal narrowing, elliptic vessel shape, acute take-off angle, intramural course, and possible concomitant coronary atherosclerosis and hemodynamics. Various cardiac imaging modalities offer unique advantages and capabilities in visualizing these anatomical and functional aspects of AAOCA. This review explored the role of noninvasive multimodality imaging in the characterization of AAOCA by highlighting the strengths, limitations, and potential applications of the current different cardiac imaging methods, with a focus on the pathophysiology of myocardial ischemia and stress testing protocols.

Coronary CT FFR vs Invasive Adenosine and Dobutamine FFR in a Right Anomalous Coronary Artery.

We present the management of an anomalous coronary artery originating from the opposite sinus of Valsalva with comprehensive diagnostic workup including noninvasive coronary computed tomography (CT) derived fractional flow reserve (FFR) and invasive dobutamine-volume challenge-FFR/intravascular ultrasound. After surgical operation, treatment success was quantified by anatomical and functional analysis in postoperative CT. (Level of Difficulty: Advanced.).

Combined Analysis of Myocardial Deformation and Oxygenation Detects Inducible Ischemia Unmasked by Breathing Maneuvers in Chronic Coronary Syndrome.

Introduction: In patients with chronic coronary syndromes, hyperventilation followed by apnea has been shown to unmask myocardium susceptible to inducible deoxygenation. The aim of this study was to assess whether such a provoked response is co-localized with myocardial dysfunction. Methods: A group of twenty-six CAD patients with a defined stenosis (quantitative coronary angiography > 50%) underwent a cardiovascular magnetic resonance (CMR) exam prior to revascularization. Healthy volunteers older than 50 years served as controls (n = 12). Participants hyperventilated for 60s followed by brief apnea. Oxygenation-sensitive images were analyzed for changes in myocardial oxygenation and strain. Results: In healthy subjects, hyperventilation resulted in global myocardial deoxygenation (-10.2 ± 8.2%, p < 0.001) and augmented peak circumferential systolic strain (-3.3 ± 1.6%, p < 0.001). At the end of apnea, myocardial signal intensity had increased (+9.1 ± 5.3%, p < 0.001) and strain had normalized to baseline. CAD patients had a similar global oxygenation response to hyperventilation (-5.8 ± 9.6%, p = 0.085) but showed no change in peak strain from their resting state (-1.3 ± 1.6%), which was significantly attenuated in comparison the strain response observed in controls (p = 0.008). With apnea, the CAD patients showed an attenuated global oxygenation response to apnea compared to controls (+2.7 ± 6.2%, p < 0.001). This was accompanied by a significant depression of peak strain (3.0 ± 1.7%, p < 0.001), which also differed from the control response (p = 0.025). Regional analysis demonstrated that post-stenotic myocardium was most susceptible to de-oxygenation and systolic strain abnormalities during respiratory maneuvers. CMR measures at rest were unable to discriminate post-stenotic territory (p > 0.05), yet this was significant for both myocardial oxygenation [area under the curve (AUC): 0.88, p > 0.001] and peak strain (AUC: 0.73, p = 0.023) measured with apnea. A combined analysis of myocardial oxygenation and peak strain resulted in an incrementally higher AUC of 0.91, p < 0.001 than strain alone. Conclusion: In myocardium of patients with chronic coronary syndromes and primarily intermediate coronary stenoses, cine oxygenation-sensitive CMR can identify an impaired vascular and functional response to a vasoactive breathing maneuver stimulus indicative of inducible ischemia.

Association of Palmar Arch Collateral Function and Radial Artery Occlusion After Transradial Access.

The prevalence and implications of radial artery occlusion (RAO) after transradial catheterization are an intensely discussed topic, resulting in numerous preventive strategies such as adjusted anticoagulation, residual-patency hemostasis, or distal puncture site. The present study aimed at assessing an association of palmar arch, in particular radial artery collateral function and RAO after transradial access (TRA) catheterization. Radial artery collateral function was determined using radial artery pressure signals in the nonobstructed vessel and during brief manual occlusion of the more proximal radial artery. Collateral flow index, the ratio of mean occlusive divided by mean nonocclusive arterial blood pressure, both subtracted by central venous pressure, was determined during manual RAO (radial artery collateral flow index [CFIrad]). The presence or absence of RAO was determined by Doppler ultrasound at least 3 months after TRA. A total of 630 patients with TRA coronary angiography underwent palmar arch, that is, radial and radial plus ulnar artery collateral function assessment. CFIrad was equal to 0.808 ± 0.144 (95% confidence interval 0.797 to 0.819). A total of 200 patients underwent Doppler ultrasound examination of their forearm arterial circulation 301 ± 140 days after TRA. Eight (4%) patients showed signs of RAO, 4 of whom (2%) had a complete RAO and 4 (2%) a stenosis above 30%. Patients with RAO showed a higher CFIrad than those without RAO: 0.900 ± 0.074 versus 0.801 ± 0.154 (p = 0.006). In conclusion, complete RAO as determined by Doppler ultrasound later than 3 months after TRA is rare (2%). In the long run, RAO appears to be related to a very well-developed radial artery collateral function.

Effect of permanent right internal mammary artery occlusion on right coronary artery supply: A randomized placebo-controlled clinical trial.

Natural, nonsurgical internal mammary artery (IMA) bypasses to the coronary circulation have been shown to function as extracardiac sources of myocardial blood supply. The goal of this randomized, placebo-controlled, double-blind trial was to test the efficacy of permanent right IMA (RIMA) device occlusion on right coronary artery (RCA) occlusive blood supply and on clinical and electrocardiographic (ECG) signs of myocardial ischemia. METHODS: This was a prospective superiority trial in 100 patients with chronic coronary artery disease randomly allocated (1:1) to RIMA vascular device occlusion (verum group) or to RIMA sham procedure (placebo group). The primary study end point was RCA collateral flow index (CFI) as obtained during a 1-minute ostial RCA balloon occlusion at baseline before and at follow-up examination 6 weeks after the trial intervention. CFI is the ratio between simultaneous mean coronary occlusive divided by mean aortic pressure both subtracted by central venous pressure. Simultaneously obtained secondary study end points were the registration of angina pectoris and quantitative intracoronary ECG ST-segment shift. RESULTS: CFI change during the follow-up period was +0.036 ±â€¯0.068 in the verum group and -0.021 ±â€¯0.097 in the placebo group (P = .0011). Angina pectoris during the same RCA balloon occlusions had disappeared at follow-up in 14/49 patients of the verum group and in 4/49 patients of the placebo group (P = .0091). Simultaneous intracoronary ECG ST-segment shift change revealed diminished myocardial ischemia at follow-up in the verum group and more severe ischemia in the placebo group. CONCLUSIONS: Permanent RIMA device occlusion augments RCA supply to the effect of diminishing clinical and electrocardiographic signs of myocardial ischemia during a brief controlled coronary occlusion.