Michael R. McMullan

Adenosine infusion increases plasma levels of VEGF in humans.

BackgroundMany in vitro studies have shown that adenosine (Ado) can induce vascular endothelial growth factor (VEGF) mRNA and protein expression and stimulate endothelial proliferation. In the present study, we seek to determine whether Ado can increase circulating levels of VEGF protein in the intact human.MethodsFive outpatients 49.3 ± 6.7 years of age and weighing 88.2 ± 8.5 kg were selected. They were given a 6 min intravenous infusion of Ado (0.14 mg kg-1 min-1) in conjunction with sestamibi myocardial perfusion scans. Mean blood pressure (MBP, calculated from systolic and diastolic values) and heart rate (HR) were determined before Ado infusion and every 2 min for the next 10 min. Plasma VEGF concentrations (ELISA) were determined immediately before Ado infusion and 1 h, 2 h, and 8 h after the infusion.ResultsPlasma VEGF concentration averaged 20.3 ± 2.0 pg ml-1 prior to Ado infusion, and increased to 62.7 ± 18.1 pg ml-1 at 1 h post- infusion (p < 0.01). VEGF plasma concentration returned to basal levels 2 h after infusion (23.3 ± 3.4 pg ml-1). MBP averaged 116 ± 7 mmHg and heart rate averaged 70 ± 7 prior to Ado infusion. MBP decreased by a maximum of ~22% and HR increased by a maximum of ~17% during the infusion.ConclusionWe conclude from these preliminary findings that intravenous infusion of adenosine can increase plasma levels of VEGF in humans.

Congenital coronary arteriovenous fistula presenting with syncope.

Previous reports of syncope in patients with coronary arteriovenous fistula (CAVF) have theorized that it occurs secondary to a coronary steal phenomenon. We present a case of syncope in a young woman with a CAVF and no anatomic substrate for coronary steal.

Delayed Time to Peak Velocity Is Useful for Detecting Severe Aortic Stenosis

Background Time to peak velocity (TPV) is an echocardiographic variable that can be easily measured and reflects a late peaking murmur, a classic physical finding suggesting severe aortic stenosis (AS). The aim of this study was to investigate the usefulness of TPV to evaluate AS severity. Methods and Results This study included 700 AS patients, whose aortic valve area (AVA) was <1.5 cm2, and 200 control patients. The TPV was defined as the time from aortic valve opening to when the flow velocity across the aortic valve reaches its peak. AS severity was classified as follows: High gradient severe AS, mean pressure gradient ≥40 mm Hg and AVA index (AVAI) <0.6 cm2/m2; Low gradient severe AS, mean pressure gradient <40 mm Hg, AVAI <0.6 cm2/m2, and dimensionless index <0.25; moderate AS, mean pressure gradient <40 mm Hg, AVAI ≥0.6 cm2/m2. The area under the receiver operating characteristic curve of TPV to predict high gradient severe AS was 0.94 (95% CI: 0.92–0.97, P<0.001). TPV was significantly delayed in low gradient severe AS compared with moderate AS both in patients with preserved (102±13 ms versus 83±13 ms, P<0.001) and with reduced ejection fraction (110±18 ms versus 88±13 ms, P<0.001). Delayed TPV was associated with increased all‐cause mortality or need for aortic valve replacement after adjustment for confounders (hazard ratio for first quartile, reference is fourth quartile: 7.31, 95% CI 4.26–12.53, P<0.001). Conclusions TPV is useful to evaluate AS severity and predict poor prognosis of AS patients.

Diagnosis of fatty liver by computed tomography coronary artery calcium score

Nonalcoholic fatty liver disease may range from simple steatosis to fibrosis and cirrhosis. It is associated with the development of coronary artery calcification and appears to be an independent predictor of future adverse cardiovascular events. As the presence of a fatty liver appears to portray an independent increased risk, it may be beneficial to note this on coronary artery calcium scoring reports. Determination of fatty liver is relatively easy to perform. We discuss the method used by the Multi‐Ethnic Study of Atherosclerosis (MESA) study for determination of fatty liver from CT coronary artery calcium scoring acquisitions, which may be implemented in clinical analysis.

Left Ventricular False Tendons are Associated With Left Ventricular Dilation and Impaired Systolic and Diastolic Function

Background: Left ventricular false tendons (LVFTs) are chord‐like structures that traverse the LV cavity and are generally considered to be benign. However, they have been associated with arrhythmias, LV hypertrophy and LV dilation in some small studies. We hypothesize that LVFTs are associated with LV structural and functional changes assessed by echocardiography. Methods: We retrospectively evaluated echocardiographic and clinical parameters of 126 patients identified as having LVFTs within the past 2 years and compared them to 85 age‐matched controls without LVFTs. Results: There were no significant differences in age (52 ± 18 versus 54 ± 18 years, P = 0.37), sex (55% versus 59% men, P = 0.49), race (36% versus 23% white, P = 0.07), systolic blood pressure (131 ± 22 versus 132 ± 23 mmHg, P = 0.76) or body mass index (BMI, 31 ± 8 versus 29 ± 10 kg/m2, P = 0.07) between controls and patients with LVFTs, respectively. Patients with LVFTs had more prevalent heart failure (43% versus 21%, P = 0.001). Patients with LVFTs had more LV dilation, were 2.5 times more likely to have moderate‐to‐severe mitral regurgitation, had more severe diastolic dysfunction and reduced LV systolic function (18% lower) compared with controls (all P < 0.05). After adjustment for covariates, basal and middle LVFT locations were associated with reduced LV systolic function (P < 0.01), and middle LVFTs were associated with LV dilation (P < 0.01). Conclusions: Our findings suggest that LVFTs may not be benign variants, and basal and middle LVFTs may have more deleterious effects. Further prospective studies should be performed to determine their pathophysiological significance and whether they play a causal role in LV dysfunction.

Coronary risk assessment using traditional risk factors with CT coronary artery calcium scoring in clinical practice

As coronary artery calcium (CAC) is atherosclerosis and not just a marker of cardiovascular (CV) disease, measurement of a patients coronary artery calcium score (CACS) is a strong predictor of risk. Clinically performed in asymptomatic patients, the CACS, along with several CV risk factors, namely age, sex, ethnicity, diabetes, tobacco use, family history, cholesterol level, blood pressure, and use of cholesterol or hypertensive medications, provide a predictive model of 10 year risk for CV events. A smartphone “App” makes this quick to obtain and use. This helps the clinician in making recommendations for both lifestyle changes and statin therapy. Those patients in which the most benefit occur from measurement of a CACS are those at an intermediate CV risk. Measurement of the CACS has become an integral part of the clinicians assessment of a patients CV risk and for guiding preventative therapies.

Coronary risk assessment using traditional risk factors with computed tomography coronary artery calcium scoring: Illustrative cases

A patients coronary artery calcium score (CACS) is a strong independent predictor of cardiovascular risk. Used in conjunction with traditional measures of risk, the CACS helps the clinician discuss cardiovascular (CV) risk and recommend therapies with the patient. We present several cases in which measurement of the CACS and traditional risk factors were used to help guide the clinician–patient conversation and guide therapies.

Identification of candidates for PFO closure in the echocardiography laboratory

A patent foramen ovale (PFO) is implicated in several pathologic processes, including that of cryptogenic stroke (cCVA). Recent trials identify “high‐risk” PFOs in patients with cCVA as likely to benefit from percutaneous closure. The younger the patient (<60 years old) the more likely a PFO may be attributable to the cCVA. The RoPE Score index helps determine the likelihood that an existing PFO is related to a cCVA. This may help guide the clinician and patient when contemplating percutaneous PFO closure. When evaluating a patient for possible percutaneous closure, one should identify the CVA as a typical ischemic type stroke. In order to “rule‐out” other causes of CVA, imaging of the intracranial arteries, cervical, and aortic arch vessels should be performed. Small vessel disease or a lacunar‐type infarct should be excluded. To rule out atrial fibrillation, prolonged monitoring should be performed. An index has been developed to determine the probability that a PFO is the causative etiology and calculates the risk of recurrence. This may help guide the clinician and patient in the decision for PFO closure. In addition, one should consider a work‐up for a hypercoagulable state. We will obtain an ultrasound of the lower extremities or consider deep pelvic vein thrombosis (prolonged sitting or malignancy). If the closure is to be performed, the Food and Drug Administration (FDA) has approved the Amplatzer PFO Occluder and the GORE Cardioform Septal Occluder for percutaneous closure. These devices are both approved in patients predominately between ages 18 and 60 years with a cCVA due to presumed paradoxical embolism as verified by a neurologist and cardiologist and when other causes of ischemic CVA have been excluded. “High‐risk” PFOs appear to achieve the most potential benefit from percutaneous closure.

Evaluation of athletes with complex congenital heart disease

As a result of improvements in congenital heart surgery, there are more adults alive today with congenital heart disease (CHD) than children. Individuals with cardiac birth defects may be able to participate in physical activities but require proper cardiovascular evaluation. The American Heart Association and American College of Cardiology released guidelines in 2015 for athletes with cardiovascular abnormalities. The guidelines express that although restriction from competitive athletics may be indicated for some, the majority of individuals with CHD can and should engage in some form of physical activity. This case study demonstrates the importance of combining all aspects of history, physical examination, ECG, and imaging modalities to evaluate cardiac anatomy and function in young athletes with complex CHD.

TREATMENT OF PSEUDO-EISENMENGER SYNDROME

Eisenmenger syndrome poses a challenging dilemma due to its high mortality and limited therapies. Though uncommon, a similar physiology has been observed which mimics Eisenmenger syndrome in presentation, yet differs dramatically in prognosis and treatment. A 55 year-old woman was admitted to a