Influence of Differential Calcification in the Descending Thoracic Aorta on Aortic Pulse Pressure

Purpose: Multiple studies have shown pulse pressure (PP) to be a strong predictor of aortic calcification. However, no studies are available that correlate PP with aortic calcification at the segmental level. Methods: We identified 37 patients with aortic PP measured during cardiac catheterization. Their noncontrast chest computed tomography scans were evaluated for the presence of calcium in different segments (ascending aorta, arch of aorta [arch], descending aorta) and quantified. Patients with calcification (Calcified Group A) were compared against patients without calcification (Noncalcified Group B) in terms of PP, calcification and compliance. Results: The mean of the total calcium score was higher in the descending aorta than the arch or ascending aorta (691 vs 571 vs 131, respectively, P < 0.0001). PP had the strongest correlation with calcification in the descending aorta (r = 0.47, P = 0.004). Calcified Group A had a much higher PP than Noncalcified Group B, with the greatest difference in the descending aorta (20 mmHg, P < 0.0001), lesser in the ascending aorta (10 mmHg, P = 0.12) and the least in the arch (5 mmHg, P = 0.38). Calcified Group A patients also had much lower compliance than Noncalcified Group B patients, with the greatest difference among groups seen in the descending aorta (0.7 mL/mmHg, P = 0.002), followed by the ascending aorta, then arch. Conclusions: These are the first data to evaluate the relative impact of aortic segments in PP. Finding the greatest amount of calcification along with greatest change in PP and compliance in the descending aorta makes a case that the descending aorta plays a major role in PP as compared to other segments of the thoracic aorta

Relative Associations of Age, Height, and Weight on Sinus of Valsalva and Mid-Ascending Aorta: An Imaging and Epidemiology Study

Background: Prior studies show ascending aorta diameter varies with age, height and weight, but they did not evaluate relative influence of these variables on aortic diameter. Since height is genetically determined, and genetic disorders like Marfan syndrome are predominantly associated with sinus of Valsalva (SOV) dilation, we hypothesized height may have stronger association with SOV. Purpose: Based on anecdotal observation, since age, weight and obesity are acquired attributes, we hypothesized age, weight and body mass index may have greater association with mid-ascending aorta (MAA) diameter, even in normal patients. Methods: We evaluated echocardiographic studies of patients ≥ 15 years old that were done in the last 4 years to measure SOV and MAA diameter in normal patients (defined as: medical records and echocardiograms did not reveal any of the 28 aortic dilation risk factors listed in the American Heart Association 2010 guidelines). Results: Of 65,843 patients, 3,201 were identified as normal. SOV measurements were available in 2,046, MAA in 2,334. Age had stronger correlation with MAA (β = 0.50; r = 0.52; P \u3c 0.001) than SOV (β = 0.33; r = 0.35; P \u3c 0.001). Weight was similarly correlated with diameters of SOV (r = 0.37; P \u3c 0.001) and MAA (r = 0.37; P \u3c 0.001). Height had stronger correlation with SOV diameter (β = 0.41; r = 0.38; P \u3c 0.001) than MAA (β = 0.26; r = 0.25; P \u3c 0.001). Conclusion: These data suggest that in normal subjects, age, weight and body mass index have stronger associations with the mid-ascending aorta, whereas height has a stronger association with the sinus of Valsalva

Aortopathy in hypertrophic cardiomyopathy; The association with sinus of valsalva versus mid ascending aorta: An epidemiological study

Background: A few prior studies have demonstrated the increased prevalence of dilated ascending aorta in patients with hypertrophic cardiomyopathy (HCM). There are no studies evaluating the relative association of HCM with sinus of Valsalva (SV) versus mid ascending aorta (MAA). In addition, the mechanism behind aortic dilation in HCM is unclear, as to whether it is acquired or genetically mediated. Methods: Echocardiography reports of patients (n= 65,843; 46.5% male), referred to tertiary care center from January 2011 to November 2014 with adequate data on aortic parameters (diameter of SV/MAA) were reviewed. Electronic medical records were queried to obtain patients with HCM using ICD 9 codes. Aortic dilation was defined based on American Society of Echocardiography guidelines published in 2015. The records were evaluated for presence of genetic studies. Results:Of the 65,843 patients, 553 HCM patients were identified, out of which 48% were men. The mean age was similar in both HCM and general population (63.7±16.5 vs. 64.3 ±17.3, p=0.384). The mean diameter of SV (3.21 ±0.51 vs. 3.08±0.46; p = Conclusions: These data suggest that HCM is associated with increased prevalence of dilated SV, but not MAA. The lower odds of dilated aorta in HCM patients who were gene positive, suggest that this association may not be genetically mediated. Further studies are required to identify the pathophysiology behind this association

Coronary Aorta Systolic and Diastolic Pressure Indices: Two Novel Indicators for Predicting Significant Coronary Stenosis –– A Validation Against Fractional Flow Reserve

Background: Since most of the coronary flow occurs in diastole, either mean Pd/Pa or iFR has been used to measure the hemodynamic significance of a coronary stenosis. We have observed that a significant pressure gradient exists in coronary stenosis even in systole, which is contrary to general understanding but similar to ankle brachial index. Furthermore, prior studies have evaluated baseline Pd/Pa (mean coronary artery/mean aorta pressure) ratio as well as iFR (instantaneous wave-free ratio obtained during entire period of diastole) to predict fractional flow reserve (FFR) ≤ 0.80. We hypothesized a simple end-systolic and -diastolic pressure measurement in the coronary artery distal to stenosis may perform adequately to predict FFR, obviating a need to measure Pd/Pa or iFR. Purpose: We sought to evaluate systolic and diastolic Pd/Pa, and termed them coronary artery systolic pressure index (CASPI) and coronary artery diastolic pressure index (CADPI), respectively, against FFR ≤ 0.80. Methods: After retrospectively identifying 555 moderate stenotic lesions undergoing FFR measurement at a tertiary care center over a 4-year period, we procured original pressure tracings obtained during the cardiac catheterization and manually measured systolic and diastolic pressures in the aorta and in the coronary artery distal to the stenosis, before and after adenosine infusion. Utilizing FFR ≤ 0.80, operating test characteristics of CASPI and CADPI were measured and compared to those of baseline Pd/Pa. Results: In the 555 lesions, mean CASPI (0.97 ± 0.04) and CADPI (0.95 ± 0.08) were similar to baseline Pd/Pa (0.95 ± 0.05). CASPI correlated well with baseline Pd/Pa (Spearman r = 0.81; P \u3c 0.0001). Similarly, CADPI was strongly correlated with baseline Pd/Pa (0.86; P \u3c 0.0001). The area under the receiver operating curve (AUC) was lower for CASPI and CADPI, as compared to baseline Pd/Pa (0.80 vs. 0.82 vs. 0.89, respectively), for predicting the FFR ≤ 0.80. For a CASPI \u3c 0.88 there were no false positives with 100% specificity, and for a CASPI \u3e 1.02, there were no false negatives with 100% sensitivity. Similarly, for a CADPI \u3c 0.8 there were no false positives with 100% specificity, and for CADPI \u3e 1.16 there were no false negatives with 100% sensitivity. Conclusion: These data demonstrate that contrary to the popular belief, significant systolic and diastolic pressure gradients distal to coronary stenosis exist with a reasonable but lower predictive power towards FFR ≤ 0.80

Coronary Aorta Systolic and Diastolic Pressure Indices: Two Novel Indicators for Predicting Significant Coronary Stenosis –– A Validation Against Fractional Flow Reserve

Background: Since most of the coronary flow occurs in diastole, either mean Pd/Pa or iFR has been used to measure the hemodynamic significance of a coronary stenosis. We have observed that a significant pressure gradient exists in coronary stenosis even in systole, which is contrary to general understanding but similar to ankle brachial index. Furthermore, prior studies have evaluated baseline Pd/Pa (mean coronary artery/mean aorta pressure) ratio as well as iFR (instantaneous wave-free ratio obtained during entire period of diastole) to predict fractional flow reserve (FFR) ≤ 0.80. We hypothesized a simple end-systolic and -diastolic pressure measurement in the coronary artery distal to stenosis may perform adequately to predict FFR, obviating a need to measure Pd/Pa or iFR. Purpose: We sought to evaluate systolic and diastolic Pd/Pa, and termed them coronary artery systolic pressure index (CASPI) and coronary artery diastolic pressure index (CADPI), respectively, against FFR ≤ 0.80. Methods: After retrospectively identifying 555 moderate stenotic lesions undergoing FFR measurement at a tertiary care center over a 4-year period, we procured original pressure tracings obtained during the cardiac catheterization and manually measured systolic and diastolic pressures in the aorta and in the coronary artery distal to the stenosis, before and after adenosine infusion. Utilizing FFR ≤ 0.80, operating test characteristics of CASPI and CADPI were measured and compared to those of baseline Pd/Pa. Results: In the 555 lesions, mean CASPI (0.97 ± 0.04) and CADPI (0.95 ± 0.08) were similar to baseline Pd/Pa (0.95 ± 0.05). CASPI correlated well with baseline Pd/Pa (Spearman r = 0.81; P \u3c 0.0001). Similarly, CADPI was strongly correlated with baseline Pd/Pa (0.86; P \u3c 0.0001). The area under the receiver operating curve (AUC) was lower for CASPI and CADPI, as compared to baseline Pd/Pa (0.80 vs. 0.82 vs. 0.89, respectively), for predicting the FFR ≤ 0.80. For a CASPI \u3c 0.88 there were no false positives with 100% specificity, and for a CASPI \u3e 1.02, there were no false negatives with 100% sensitivity. Similarly, for a CADPI \u3c 0.8 there were no false positives with 100% specificity, and for CADPI \u3e 1.16 there were no false negatives with 100% sensitivity. Conclusion: These data demonstrate that contrary to the popular belief, significant systolic and diastolic pressure gradients distal to coronary stenosis exist with a reasonable but lower predictive power towards FFR ≤ 0.80

Relative associations of age, height and weight on sinus of valsalva and mid ascending aorta: an imaging and epidemiology study

Background: Prior studies show ascending aorta diameter varies with age, height and weight, but they did not evaluate relative influence of these variables on aortic diameter. Since height is genetically determined, and genetic disorders like Marfan syndrome are predominantly associated with sinus of Valsalva (SOV) dilation, we hypothesized height may have stronger association with SOV. Purpose: Based on anecdotal observation, since age, weight and obesity are acquired attributes, we hypothesized age, weight and body mass index may have greater association with mid-ascending aorta (MAA) diameter, even in normal patients. Methods: We evaluated echocardiographic studies of patients ≥ 15 years old that were done in the last 4 years to measure SOV and MAA diameter in normal patients (defined as: medical records and echocardiograms did not reveal any of the 28 aortic dilation risk factors listed in the American Heart Association 2010 guidelines). Results: Of 65,843 patients, 3,201 were identified as normal. SOV measurements were available in 2,046, MAA in 2,334. Age had stronger correlation with MAA (β = 0.50; r = 0.52; P \u3c 0.001) than SOV (β = 0.33; r = 0.35; P \u3c 0.001). Weight was similarly correlated with diameters of SOV (r = 0.37; P \u3c 0.001) and MAA (r = 0.37; P \u3c 0.001). Height had stronger correlation with SOV diameter (β = 0.41; r = 0.38; P \u3c 0.001) than MAA (β = 0.26; r = 0.25; P \u3c 0.001). Conclusion: These data suggest that in normal subjects, age, weight and body mass index have stronger associations with the mid-ascending aorta, whereas height has a stronger association with the sinus of Valsalva

Distal dicrotic notch in the coronary artery pressure waveform predicts significant stenosis, as validated by fractional flow reserve, but performs inferiorly as compared to pd/pa

Background: A single small prior study (n=97) has suggested that absence of distal dicrotic notch (DDN) in the coronary artery, distal to an intermediate stenosis, may indicate a significant stenosis, proven by an abnormal fractional flow reserve (FFR). This finding has neither been evaluated by other studies nor compared against other, more established, non hyperemic indices like Pd/Pa (distal coronary pressure/proximal coronary pressure). Methods: Of the 926 FFR measurements performed in a large tertiary care center over last 4 years, we included 454 measurements with adequate baseline tracing data. After excluding 49 due to absence of aortic dicrotic notch, 405 patients had their tracings printed with pre-adenosine measurement with 8 cardiac cycles and dicrotic notch was characterized visually into four types, i.e., full notch, partial notch, definite change in angle of descending limb at the end of systole, and absent DDN, by two different observers. Operating test characteristics of dicrotic notch were measured against the criterion standard of FFR ≤0.8 to detect significant ischemia. Results:Out of 405 patients, 43 had absent DDN. The mean FFR in those with absent DDN was significantly lower (0.79 versus 0.86; p= Conclusions: While an absent DDN is associated with an abnormal FFR, our data suggest meaningfully lower performance in prediction of an abnormal FFR as compared to Pd/Pa, indicating that Pd/Pa should be preferred over DDN in clinical practice

Thoracic aortic dilatation is a hereditary disease: A large cross sectional imaging study

Background: A prior small case control study had suggested that Ascending Aortic Aneurysm (AAA) is an inherited disease followed by multiple small studies on the genetic basis of the disease. A recent large observational study evaluated diabetes to have a protective role against AAA. However, there is a lack of studies that evaluate multiple risk factors in the same study population. Methods: The echocardiography database of a large tertiary care center was electronically evaluated, over 4 years, in adults \u3e15 years of age. AAA was defined as a sinus of Valsalva dilation, based on age, sex and BSA indexed definition recommended by American Society of Echocardiography. The presence of 24 risk factors of AAA were assessed in the electronic medical record. Results: Of 37,914 patients, there were 1,035 cases of AAA, with 662 (64%) men. The study population comprised of hereditary risk factors including Marfan Syndrome (26; 0.06%), coarctation of aorta (CoA; 17; 0.05%), bicuspid aortic valve (BAV; 192; 0.5%), polycystic kidney disease (PCKD; 64; 0.17%) and hypertrophic cardiomyopathy (HCM; 249; 0.66%), as well as acquired risk factors including cocaine use (219; 0.58%), smoking (20,674; 55.6%), dyslipidemia (21,273; 56.1%), diabetes mellitus (9,774; 25.8%), aortic valve disease (3,507; 9.3%) and hypertension (24,156; 63.7%). The risk factors of developing AAA in descending order of strength of odds ratio were Marfan syndrome (6.5), CoA (4.8), BAV(4.2), cocaine use (2.5), PCKD (2.4), HCM (2.4), male gender (2.2) and aortic valve disease (2.0). The risk factors of atherosclerotic disease which include age \u3e 65, diabetes mellitus and dyslipidemia were found to have a negative association, whereas smoking and hypertension had null effect. These associations persisted in multivariate logistic regression models. Conclusions: Out of top 10 risk factors of AAA, only three 3 are not purely inherited. The traditional atherosclerotic risk factors either have null effect on AAA, or have a paradoxical relationship. These data further support the hypothesis that AAA might indeed be a hereditary disease

Dilated mid-ascending aorta in hypertrophic cardiomyopathy is associated with dynamic left ventricular outflow tract obstruction and not with genetic abnormalities

BACKGROUND: Prior studies have suggested a relationship between aortic dilatation and hypertrophic cardiomyopathy (HCM). There are no data evaluating the relative strength of association between dilated aorta and HCM in terms of whether the dilatation was mediated by left ventricular outflow tract (LVOT) obstruction or due to hereditary factors. METHODS: We retrospectively reviewed the medical and echocardiography records of the 175 patients with HCM seen and characterized by AJT in a tertiary-care HCM center. Of these, 124 received genetic testing. The patients (n=175) were categorized to have significant LVOT obstruction if the baseline dynamic LVOT gradient was \u3e20 mmHg. All the patients underwent measurement of the sinus of Valsalva (SV) and mid ascending aorta (mAA) with leading edge-to-leading edge technique in diastole. The aorta was defined as dilated if it was \u3e4 cm in the SV or mAA. RESULTS: Out of the 124 patients tested, 56 (45%) were found to be gene-positive. The most common gene abnormalities detected were mutations in MYBPC3 (22%), MYH7 (13%) and TNNT2 (0.2%). Out of all 175 patients, the mean LVOT gradient was 24±34 and a range of 0-160 mmHg, with 49 patients having a gradient \u3e20 mmHg. The gene-negative patients had a higher mean dilated SV (3.39 cm vs 3.12 cm; P=0.0038) and dilated mAA (3.3 cm vs 3 cm; P=0.005) than gene-positive patients (n=56). Gene-positive patients had a slightly lower prevalence of dilated SV (11% vs. 15%) and mAA (7% vs. 10%), which was not statistically significant. Patients with a baseline LVOT gradient ≥20 mmHg had a 4 times higher prevalence (16% vs 4%) of dilated mAA (\u3e4 cm) than those with LVOT gradient of \u3c20 mmHg (OR: 4.1, 95% CI 1.17-14.4, P=0.019), whereas no significant relationship was seen with dilated SV (OR: 1.7, 95% CI 0.61-4.8, P=0.3). This association with dilated mAA persisted after adjusting for hypertension, aortic stenosis, aortic regurgitation and aortic prosthesis in stratified and multivariate analyses. CONCLUSIONS: The dilatation of mAA in patients with HCM appears to be more strongly associated with baseline dynamic LVOT obstruction than with genetic abnormalities