Cardiology

Van Meter, C., A. Vasudevan, J. M. Cuccerre and J. M. Schussler (2018). “Time to discharge following diagnostic coronary procedures via transradial artery approach: A comparison of Terumo band and StatSeal hemostasis.” Cardiovasc Revasc Med Mar 24. [Epub ahead of print].

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BACKGROUND: The transradial artery (TRA) approach for cardiac catheterization is associated with fewer complications, earlier mobilization and a shorter stay at the hospital. The objective of this study was to determine whether hemostasis with a combination of a compression band (Terumo TR band) and a hemostatic patch (StatSeal) decreases the time to discharge from the hospital compared to the Terumo (TR) band alone in patients undergoing diagnostic coronary catheterizations through a TRA approach. METHODS: We retrospectively looked at 445 patients who underwent diagnostic coronary angiography through the TRA approach at the Jack and Jane Hamilton Heart and Vascular Hospital, Dallas, Texas between July 2016 and June 2017. The difference in the time to discharge between the two groups was assessed by a Wilcoxon Rank-sum test. RESULTS: The combination of a TR band and a StatSeal hemostatic patch was used in 70.3% (313) of the patients. Comparison of the two groups demonstrated a statistically significant reduction in time from the end of the procedure to discharge (p<0.001), with no significant alteration in safety among those with a combination of TR band and a StatSeal hemostatic patch. CONCLUSION: With increasing frequency of TRA procedures in the United States, we demonstrate one effective method to significantly reduce the time to radial hemostasis and reduce the time to patient discharge from the hospital.

Rangaswami, J., M. Naranjo and P. A. McCullough (2018). “Preeclampsia as a Form of Type 5 Cardiorenal Syndrome: An Underrecognized Entity in Women’s Cardiovascular Health.” Cardiorenal Med 8(2): 160-172.

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BACKGROUND: Preeclampsia is a multisystem vascular disorder of pregnancy that remains a leading cause of maternal and fetal morbidity and mortality. Preeclampsia remains an underrecognized risk factor for future cardiovascular and kidney disease in women and represents the confluence of preexisting vascular risk factors with superimposed endothelial injury from placental mediated anti-angiogenic factors. SUMMARY: This review highlights the close relationship between preeclampsia and future cardiovascular and kidney disease. It describes the pathophysiology and current understanding of biomarkers that form the molecular signature for long-term endothelial dysfunction in preeclamptic women. Finally, it describes strategies for early identification and management of women with preeclampsia with elevated risk for cardiovascular and kidney disease. Key Messages: Future rigorous studies on cardiovascular risk modification in this phenotype of disease are essential to reduce the burden of cardiovascular and kidney disease, in women with preeclampsia.

Roberts, W. C. (2018). “Cardiac rupture during acute myocardial infarction diagnosed clinically.” Coron Artery Dis 29(2): 95-96.

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Rencuzogullari et al. from Kars, Izmir, and Istanbul, Turkey, compared clinical observations in 33 patients with cardiac rupture during acute myocardial infarction (AMI) to observations in 1630 patients, also with AMI but without clinical evidence of cardiac rupture. Compared with the patients without cardiac rupture, those with rupture had a greater percent in Kilip classes II–IV: higher leukocyte counts, higher levels of C-reactive protein, creatinine kinase MB, and peak troponin I; higher frequencies of the thrombus in the left anterior descending coronary artery, higher basal syntax scores, and syntax II percutaneous coronary intervention scores. The systolic blood pressures, glomerular filtration rates, left ventricular ejection fractions, and hemoglobin values were lower. Many of these relations have not been described previously in patients with AMI and cardiac rupture compared with those with AMI but without cardiac rupture. All patients in their study underwent percutaneous coronary intervention, a procedure that may have effects on some of these factors. What are some potential and real problems with this clinical study? Cardiac rupture during AMI is not easily diagnosed clinically, particularly when the rupture site is the left ventricular free wall, the most common rupture site during AMI. Some cases in this clinical study classified as cardiac rupture probably did not have cardiac rupture, and some cases classified as no cardiac rupture probably did have cardiac rupture. Autopsies were not done in any of their patients or, if so, the results of such studies were not reported. Autopsy or surgery, in actuality, may be the only means of accurately diagnosing cardiac rupture if it involves the left ventricular free wall. A relatively high early survival rate (nearly 50% at 30 days) in their rupture cases also raises some doubt of the accuracy of their diagnosis of rupture during life. The type of cardiac rupture was not specified by these authors, namely whether it involved the left ventricular free wall or ventricular septum or a papillary muscle. The latter two are far less frequent than the former and the former is much more difficult to diagnose clinically than the latter two. It might be useful to compare some findings in autopsy-documented cases of cardiac rupture secondary to AMI to autopsy-documented cases of AMI without cardiac rupture. Table 1 summarizes a number of studies 2–15 performed by me and my colleagues, and Table 2 focuses on factors distinguishing cardiac rupture cases from nonruptured autopsy cases during AMI 2–I15. I suspect that some of the observations of the present authors that are at variance with previous principles learned in patients studied at autopsy with cardiac rupture during AMI are probably related to errors in diagnosis of cardiac rupture. As mentioned, left ventricular free wall rupture is by far the most common site of cardiac rupture during AMI and it is often impossible to get an echocardiogram recorded to search for hemopericardium before the fatality occurs. Nevertheless, the authors made a valiant attempt to diagnose cardiac rupture clinically and to compare numerous variables to their nonrupture cases. Such studies are not easy particularly when the ‘instruments of precision’ are less than ideal when diagnosing cardiac rupture secondary to AMI clinically. (Excerpt from text, p. 95; no abstract available.)

Pollock, B. D., E. W. Harville, K. T. Mills, W. Tang, W. Chen and L. A. Bazzano (2018). “Cardiovascular Risk and the American Dream: Life Course Observations From the BHS (Bogalusa Heart Study).” J Am Heart Assoc 7(3).

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BACKGROUND: Economic literature shows that a child’s future earnings are predictably influenced by parental income, providing an index of “socioeconomic mobility,” or the ability of a person to move towards a higher socioeconomic status from childhood to adulthood. We adapted this economic paradigm to examine cardiovascular risk mobility (CRM), or whether there is life course mobility in relative cardiovascular risk. METHODS AND RESULTS: Participants from the BHS (Bogalusa Heart Study) with 1 childhood and 1 adult visit from 1973 to 2016 (n=7624) were considered. We defined population-level CRM as the rank-rank slope (beta) from the regression of adult cardiovascular disease (CVD) risk percentile ranking onto childhood CVD risk percentile ranking (beta=0 represents complete mobility; beta=1 represents no mobility). After defining and measuring relative CRM, we assessed its correlation with absolute cardiovascular health using the American Heart Association’s Ideal Cardiovascular Health metrics. Overall, there was substantial mobility, with black participants having marginally better CRM than whites (betablack=0.10 [95% confidence interval, 0.05-0.15]; betawhite=0.18 [95% confidence interval, 0.14-0.22]; P=0.01). Having high relative CVD risk at an earlier age significantly reduced CRM (betaagexslope=-0.02; 95% confidence interval, -0.03 to -0.01; P<0.001). Relative CRM was strongly correlated with life course changes in Ideal Cardiovascular Health sum (r=0.62; 95% confidence interval, 0.60-0.65). CONCLUSIONS: Results from this novel application of an economic mobility index to cardiovascular epidemiology indicated substantial CRM, supporting the paradigm that life course CVD risk is highly modifiable. High CRM implies that the children with the best relative CVD profiles may only maintain a slim advantage over their peers into adulthood.

Packer, M. (2018). “Worsening Heart Failure During the Use of DPP-4 Inhibitors: Pathophysiological Mechanisms, Clinical Risks, and Potential Influence of Concomitant Antidiabetic Medications.” JACC Heart Fail. Mar 1. [Epub ahead of print].

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Although dipeptidyl peptidase (DPP)-4 inhibitors have been reported to have a neutral effect on thromboembolic vaso-occlusive events in large-scale trials, they act to potentiate several endogenous peptides that can exert deleterious cardiovascular effects. Experimentally, DPP-4 inhibitors may augment the ability of glucagon-like peptide-1 to stimulate cyclic adenosine monophosphate in cardiomyocytes, and potentiation of the effects of stromal cell-derived factor-1 by DPP-4 inhibitors may aggravate cardiac fibrosis. These potentially deleterious actions of DPP-4 inhibitors might not become clinically apparent if these drugs were to promote sodium excretion. However, the natriuretic effect of DPP-4 inhibitors is modest, because they act on the distal (rather than proximal) renal tubules. Accordingly, both clinical trials and observational studies have reported an increase in the risk of heart failure in patients with type 2 diabetes who were receiving DPP-4 inhibitors. This risk may be muted in trials with a high prevalence of metformin use or with low and declining background use of insulin and thiazolidinediones. Still, the most vulnerable patients (i.e., those with established heart failure) were not well represented in these studies. The only trial that specifically evaluated patients with pre-existing left ventricular dysfunction observed important drug-related adverse structural and clinical effects. In conclusion, an increased risk of worsening heart failure appears to be a class effect of DPP-4 inhibitors, even in patients without a history of heart failure. Additional clinical trials are urgently needed to elucidate the benefits and risks of DPP-4 inhibitors in patients with established left ventricular dysfunction.