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Background Perfusion defects during stress can occur in hypertrophic cardiomyopathy (HCM) from either structural or functional abnormalities of the coronary microcirculation. In this study, vasodilator stress myocardial contrast echocardiography (MCE) was used to quantify and spatially characterize hyperemic myocardial blood flow (MBF) deficits in HCM. Methods Regadenoson stress MCE was performed in patients with septal-variant HCM (n = 17) and healthy control subjects (n = 15). The presence and spatial distribution (transmural diffuse, patchy, subendocardial) of perfusion defects was determined by semiquantitative analysis. Kinetic analysis of time-intensity data was used to quantify MBF, microvascular flux rate (β), and microvascular blood volume. In patients undergoing septal myectomy (n = 3), MCE was repeated > 1 years after surgery.  Results In HCM subjects, perfusion defects during stress occurred in the septum in 80%, and in non-hypertrophied regions in 40%. The majority of septal defects (83%) were patchy or subendocardial, while 67% of non-hypertrophied defects were transmural and diffuse. On quantitative analysis, hyperemic MBF was approximately 50% lower (p < 0.001) in the hypertrophied and non-hypertrophied regions of those with HCM compared to controls, largely based on an inability to augment β, although hypertrophic regions also had blood volume deficits. There was no correlation between hyperemic MBF and either percent fibrosis on magnetic resonance imaging or outflow gradient, yet those with higher degrees of fibrosis (≥ 5%) or severe gradients all had low septal MBF during regadenoson. Substantial improvement in hyperemic MBF was observed in two of the three subjects undergoing myectomy, both of whom had severe pre-surgical outflow gradients at rest. Conclusion Perfusion defects on vasodilator MCE are common in HCM, particularly in those with extensive fibrosis, but have a different spatial pattern for the hypertrophied and non-hypertrophied segments, likely reflecting different contributions of functional and structural abnormalities. Improvement in hyperemic perfusion is possible in those undergoing septal myectomy to relieve obstruction.  Trial registration ClinicalTrials.gov NCT02560467. Graphical Abstract

Cardiovascular diseases and cancer represent the two most common causes of morbidity and mortality in industrialized countries. With the increase in long-term survival of cancer patients, cardiovascular diseases are the leading cause of mortality for many cancer survivors. In this article, we will review the most common cardiovascular toxicities of cancer therapies and will describe the role of cardiac CT in the detection and monitoring of cardiovascular disease. While there is limited evidence for the use of CT imaging in cancer patients, we will discuss the utility of cardiac CT in the detection and management of coronary artery disease, pericardial and valvular heart disease.

Background: Perfusion defects during stress can occur in hypertrophic cardiomyopathy (HCM) from either structural or functional abnormalities of the coronary microcirculation. In this study, vasodilator stress myocardial contrast echocardiography (MCE) was used to quantify and spatially characterize hyperemic myocardial blood flow (MBF) deficits in HCM.Methods: Regadenoson stress MCE was performed in patients with septal-variant HCM (n=17) and healthy control subjects (n=15). The presence and spatial distribution (transmural diffuse, patchy, subendocardial) of perfusion defects was determined by semiquantitative analysis. Kinetic analysis of time-intensity data was used to quantify MBF, microvascular flux rate (b), and microvascular blood volume. In patients undergoing septal myectomy (n=3), MCE was repeated >1 years after surgery.Results: In HCM subjects, perfusion defects during stress occurred in the septum in 80%, and in non-hypertrophied regions in 40%. The majority of septal defects (83%) were patchy or subendocardial, while 67% of non-hypertrophied defects were transmural and diffuse. On quantitative analysis, hyperemic MBF was approximately 50% lower (p<0.001) in the hypertrophied and non-hypertrophied regions of those with HCM compared to controls, largely based on an inability to augment b, although hypertrophic regions also had blood volume deficits. There was no correlation between hyperemic MBF and either percent fibrosis on magnetic resonance imaging or outflow gradient, yet those with higher degrees of fibrosis (≥5%) or severe gradients all had low septal MBF during regadenoson. Substantial improvement in hyperemic MBF was observed in two of the three subjects undergoing myectomy, both of whom had severe pre-surgical outflow gradients at rest.Conclusion: Perfusion defects on vasodilator MCE are common in HCM, particularly in those with extensive fibrosis, but have a different spatial pattern for the hypertrophied and non-hypertrophied segments, likely reflecting different contributions of functional and structural abnormalities. Improvement in hyperemic perfusion is possible in those undergoing septal myectomy to relieve obstruction.Trial Registration: ClinicalTrials.gov NCT02560467.

Background Coronary slow flow phenomenon (CSFP), also called as syndrome Y is characterized by the delayed passage of contrast distally when injected into the epicardial coronaries. It accounts for upto 7% of patients undergoing coronary angiogram (CAG) for angina. Conventionally, it is determined by the coronary filling time. We aimed to determine whether coronary emptying time is a significant predictor of the coronary slow flow. Purpose To determine the coronary artery filling time and emptying time at prespecified vascular landmarks in patients with chest pain and normal epicardial coronaries. To determine the association of coronary arterial filling time and emptying time in patients with coronary slow flow phenomenon. To determine the association of various conventional coronary artery disease risk factors and various clinical parameters in patients with coronary slow flow phenomenon. Methods Patients with angina, having normal epicardial coronaries on CAG were selected consecutively between January 2019 and December 2020. Each angiogram was assessed for the coronary filling and emptying times at prespecified standard vascular landmarks on the basis of TIMI frame counts (TFC). Results A total of 37 patients with normal epicardial coronaries were analyzed, out of which 27 patients had slow flow in LAD and 17 patients had slow flow in RCA (10 had normal flow in LAD and 12 had normal flow in RCA). Eight had non dominant RCA, which were too small for analyzing TFC were excluded from the study. We observed positive correlation of coronary filling times and emptying times, both in LAD (R-Sq 0.24) and RCA (R-Sq 0.05) in slow flow patients unlike those with normal flow. We found the filling times and emptying times are significantly prolonged in slow flow patients [with mean CTFC values of 77.94 & 92.85 in LAD and 36.91 & 120.82 in RCA, respectively (P&lt;0.05)]. The capillary and venous transit time is prolonged both in LAD and RCA slow flow groups, which was of statistical significance in the RCA slow flow group (P&lt;0.05), but not in LAD slow flow group (P=0.43). We observed slow flow significantly more in male population (P=0.02) and associated with high LDL/HDL ratios and high triglycerides. Conclusion 1. In addition to coronary artery filling times, Coronary artery emptying time is an independent and significant predictor of coronary slow flow phenomenon. 2. Capillary and venous transit time is significantly prolonged in patients with slow flow in RCA whereas in patients with LAD slow flow there is non significant prolongation of capillary and venous transit time. 3. There is a positive correlation of coronary emptying time with coronary filling time in Coronary Slow Flow. This correlation is not seen in patients with normal coronary flow. 4. Coronary slow flow is observed significantly more in male population. 5. Coronary slow flow is significantly associated with high LDL/HDL ratios and triglyceride levels. Funding Acknowledgement Type of funding sources: None. Study designAngiographic landmarks for LAD and RCA – Pictorial representation