The objective of this study was to determine the optimal assessment of arterial stiffness that relates to diastolic dysfunction. Forty-one patients had measurements of brachial-ankle pulse wave velocity (baPWV), carotid-femoral pulse wave velocity (cfPWV), ankle brachial index (ABI), pulse pressure (PP), and augmentation index (AIx). Diastolic dysfunction was evaluated by echocardiographic indices of the ratio of the peak early diastolic mitral valve velocity and the peak late diastolic velocity (<i  >E/A</i> ratio), left atrial diameter, and left atrial volume indexes. There was a significant (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M1" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x1D443" d="M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5&#xA;t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z" /></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><path id="x3C" d="M512 -3l-437 233v51l437 233v-58l-378 -200v-2l378 -199v-58z" /></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><path id="x30" d="M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105&#xA;q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z" /></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><path id="x2E" d="M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z" /></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><path id="x35" d="M153 550l-26 -186q79 31 111 31q90 0 141.5 -51t51.5 -119q0 -93 -89 -166q-85 -69 -173 -71q-32 0 -61.5 11.5t-41.5 23.5q-18 17 -17 34q2 16 22 33q14 9 26 -1q61 -50 124 -50q60 0 93 43.5t33 104.5q0 69 -41.5 110t-121.5 41q-53 0 -102 -20l38 305h286l6 -8&#xA;l-26 -65h-233z" /></g>

		
	
</svg>) correlation between baPWV and <i  >E/A</i> ratio with an inverse relationship indicating that higher arterial stiffness was associated with greater diastolic dysfunction. In contrast, there was no significant correlation between <i  >E/A</i> ratio and cfPWV, PP, ABI, or AIx. After multivariate analysis, the relationship between baPWV and <i  >E/A</i> ratio remained significant (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M2" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x35"/></g>

		
	
</svg>), independent of age and systolic blood pressure (BP). There were no correlations between any index of vascular stiffness and left atrial dimension or volume. In summary, baPWV correlates with diastolic dysfunction, independent of a patient&#x2019;s age and BP and is a better indicator of diastolic dysfunction than other indicators of arterial stiffness. baPWV has the utility of infering the presence of left ventricular diastolic dysfunction.

Bryan Chow

Simon W. Rabkin

Brachial-Ankle Pulse Wave Velocity Is the Only Index of Arterial Stiffness That Correlates with a Mitral Valve Indices of Diastolic Dysfunction, but No Index Correlates with Left Atrial Size


				The aim of this study was to evaluate HRV in children requiring intensive care unit stays due to TCA poisoning between March 2009 and July 2010. In the time-domain nonspectral evaluation, the SDNN  (<svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M1" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x1D443" d="M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5&#xA;t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z" /></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><path id="x3C" d="M512 -3l-437 233v51l437 233v-58l-378 -200v-2l378 -199v-58z" /></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><path id="x30" d="M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105&#xA;q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z" /></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><path id="x2E" d="M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z" /></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><path id="x31" d="M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z" /></g>

		
	
</svg>), SDNNi (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M2" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><path id="x35" d="M153 550l-26 -186q79 31 111 31q90 0 141.5 -51t51.5 -119q0 -93 -89 -166q-85 -69 -173 -71q-32 0 -61.5 11.5t-41.5 23.5q-18 17 -17 34q2 16 22 33q14 9 26 -1q61 -50 124 -50q60 0 93 43.5t33 104.5q0 69 -41.5 110t-121.5 41q-53 0 -102 -20l38 305h286l6 -8&#xA;l-26 -65h-233z" /></g>

		
	
</svg>), RMSDD (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M3" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>), and pNN50 (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M4" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) were found to be significantly lower in the TCA intoxication group. The spectral analysis of the data recorded during the first 5 minutes after intensive care unit admission showed that the values of the nLF (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M5" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x35"/></g>

		
	
</svg>) and the LF/HF ratio (<svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M6" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><path id="x3D" d="M535 323h-483v50h483v-50zM535 138h-483v50h483v-50z" /></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) were significantly higher in the TCA intoxication group, while the nHF (<svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M7" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) values were significantly lower. The frequency-domain spectral analysis of the data recorded during the last 5 minutes showed a lower nHF (<svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M8" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) in the TCA intoxication group than in the controls, and the LF/HF ratio was significantly higher (<svg     style="vertical-align:-0.1638pt;width:58.712502px;" id="M9" height="11.375" version="1.1" viewBox="0 0 58.712502 11.375" width="58.712502"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x35"/></g>

		
	
</svg>) in the intoxication group. The LF/HF ratio was higher in the seven children with seizures (<svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M10" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><use xlink:href="#x1D443"/></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><use xlink:href="#x3C"/></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><use xlink:href="#x2E"/></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>). These findings provided us with a starting point for the value of HRV analysis in determining the risk of arrhythmia and convulsion in TCA poisoning patients. HRV can be used as a noninvasive testing method in determining the treatment and prognosis of TCA poisoning patients.

Ener Cagri Dinleyici

Zubeyir Kilic

Sabiha Sahin

Rabia Tutuncu-Toker

Makbule Eren

Zeynel Abidin Yargic

Pelin Kosger

Birsen Ucar

Heart Rate Variability in Children with Tricyclic Antidepressant  Intoxication

Natig Gassanov

Evren Caglayan

Firat Duru

Fikret Er

Atrial Fibrillation

Dynamics of blood pressure (BP) and heart rate (HR) was traced by automatic monitoring every 30&#x2009;min uninterruptedly along several months in a patient suffering from combined atrial fibrillation and heart failure during the development of disease and its therapeutic and surgical treatment (pacemaker implanting and atrioventricular ablation). Analyses of spectral components as well as signal&#x2019;s shape revealed instabilities in circadian and semicircadian parameters. A new approach for signal&#x2019;s form description without using cosine approximation is suggested. The meaning that referring a patient as dipper, night peaker, or nondipper might be useful at choosing tactics of his treatment is impugned, because all these &#x201c;types&#x201d; can transform themselves in the same person in few days. Optimization timing of treatment provides better results if not the &#x201c;types&#x201d; of daily profile would be taken to account but the real form of the BP-signal and timing its first and second derivatives.

Sergey Chibisov

George Katinas

Inna Brodskaya

Aleksandr Ertman

Grigory Gromyko

Aleksandra Konradi

Oleg Mamontov

Anna Merkuryeva

Ekaterina Polunicheva

Evgeny Shlyakhto

Anna Soboleva

Sergey Yashin

Bharadva Bhavdip

Chronobiological Analysis of Blood Pressure in a Patient with Atrial Fibrillation at the Development of Heart Failure and Its Therapeutic and Surgical Treatment

<i>Background</i>. Acute Coronary Syndrome (ACS) is a clinical condition encompassing ST Segment Elevation Myocardial Infarction (STEMI), Non-ST Segment Elevation Myocardial Infarction (NSTEMI), and Unstable Angina (UA) and is characterized by ruptured coronary plaque, ischemic stress, and/or myocardial injury. Emergency department (ED) physicians are on the front lines of ACS management. The role of new antiplatelet agents ticagrelor and prasugrel in acute ED management of ACS has not yet been defined. <i>Objective</i>. To critically review clinical trials using ticagrelor and prasugrel in the treatment of ACS and inform practitioners of their potential utility in treating ACS in the ED. <i>Results</i>. Trials on the efficacy of ticagrelor and prasugrel achieve statistical significance in decreasing composite endpoints in select patient populations. <i>Conclusion</i>. The use of ticagrelor and prasugrel as first line ED treatment of ACS is not well established. Current evidence supports the use of several agents with the final decision based on treatment protocols conjointly developed between cardiology and emergency medicine (EM). Further clinical trials involving head-to-head trials or comparisons of drug-based strategies are required to show superiority in reducing cardiac endpoints with regard to ED initiation of treatment.

M. Curial

E. Nath

E. Lang

Novel Antiplatelet Agent Use for Acute Coronary Syndrome in the Emergency Department: A Review

Dual antiplatelet therapy with aspirin and a P2Y<sub>12</sub> receptor inhibitor represents the cornerstone therapy for patients with acute coronary syndromes or undergoing percutaneous interventions, leading to a reduction of subsequent ischemic events. Variable response to clopidogrel has received close attention, and pharmacokinetic, pharmacodynamic, and pharmacogenomic factors have been identified as culprits. This led to the introduction of newer, potentially safer, and more effective antiplatelet agents (prasugrel and ticagrelor).  Additionally, several point-of-care assays of platelet function have been developed in recent years to rapidly screen individuals on antiplatelet therapy. While the routine use of platelet function testing is uncertain and not currently recommended, it may be useful in instances when the degree of platelet inhibition may be uncertain such as high-risk patients undergoing percutaneous coronary intervention or when there may be a suspected pharmacodynamic interaction with other drugs. The current paper focuses on the P2Y<sub>12</sub> receptor inhibitors and their pharmacogenetics and indications in patients with acute coronary syndromes or receiving percutaneous coronary interventions as well as the applicability of platelet function testing in this clinical context.

Adriana Dana Oprea

Wanda M. Popescu


					<svg style="vertical-align:-3.276pt" height="15.25" version="1.1" viewBox="0 0 40.674999 15.25" width="40.674999" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x50" d="M46 650h247q112 0 169 -41q64 -49 64 -141q0 -91 -56.5 -143t-138.5 -62q-23 -3 -45 -1l-74 19v-157q0 -63 15.5 -77t83.5 -19v-28h-271v28q60 5 74 20t14 77v400q0 65 -12.5 79t-69.5 18v28zM212 559v-245q31 -12 73 -12q59 0 102 38t43 124q0 77 -42.5 115.5&#xA;t-108.5 38.5q-44 0 -56 -12q-11 -8 -11 -47z" /></g><g transform="matrix(.017,-0,0,-.017,9.633,11.112)"><path id="x32" d="M412 140l28 -9q0 -2 -35 -131h-373v23q112 112 161 170q59 70 92 127t33 115q0 63 -31 98t-86 35q-75 0 -137 -93l-22 20l57 81q55 59 135 59q69 0 118.5 -46.5t49.5 -122.5q0 -62 -29.5 -114t-102.5 -130l-141 -149h186q42 0 58.5 10.5t38.5 56.5z" /></g><g transform="matrix(.017,-0,0,-.017,17.792,11.112)"><path id="x59" d="M620 650v-28q-51 -6 -70.5 -19t-48.5 -60q-68 -110 -126 -219q-17 -32 -17 -63v-136q0 -63 15.5 -77.5t84.5 -19.5v-28h-282v28q67 5 82 19.5t15 77.5v133q0 22 -21 60l-126 219q-31 53 -49 67t-62 18v28h239v-28q-51 -6 -59.5 -18t8.5 -36q13 -25 135 -237&#xA;q87 155 119 225q18 37 9 48.5t-67 17.5v28h221z" /></g><g transform="matrix(.012,-0,0,-.012,28.575,15.187)"><path id="x31" d="M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z" /></g><g transform="matrix(.012,-0,0,-.012,34.286,15.187)"><use xlink:href="#x32"/></g></svg> Receptor Inhibitors in Acute Coronary Syndromes: What Is New on the Horizon?

<i>Background</i>. Although our comprehension of nonrheumatic aortic stenosis (NRAS) has increased substantially during the last decade, less is known about the histopathology of rheumatic aortic stenosis (RAS). The aim of this study was to investigate rheumatic aortic stenosis by means of analyses previously used in nonrheumatic stenosis. <i>Material and Methods</i>. Valve specimens were obtained from 39 patients referred to hospital due to significant aortic stenosis. According to established macroscopic criteria the valves were divided into two groups consisting of 29 NRAS and 10 RAS valves. Mononuclear inflammatory cells and apolipoproteins were investigated using immunohistochemical analyses. <i>Results</i>. The localisation of calcification differed in tricuspid nonrheumatic valves when compared to bicuspid nonrheumatic and rheumatic valves. The RAS valves revealed a lower degree of T lymphocyte infiltration compared with the NRAS valves. Infiltration of macrophages was seen in all valves and there were no differences regarding deposition of apolipoprotein. <i>Conclusion</i>. Rheumatic and nonrheumatic aortic stenotic valves show a similar and significant chronic inflammation. The similarities regarding the localisation of calcification indicate that the valve anomaly/morphology can influence the pathogenesis of aortic stenosis. Finally, our findings highlight the question of a postinflammatory valvular disease of other causes than rheumatic fever.

Lars Wallby

Thora Steffensen

Lena Jonasson

Mats Broqvist

Inflammatory Characteristics of Stenotic Aortic Valves: A Comparison between Rheumatic and Nonrheumatic Aortic Stenosis

<i  >Background</i>. The <i  >CYP2C19&#x2a;2</i> allele may be associated with a reduced antiplatelet effect for clopidogrel. Here, we assessed whether <i  >CYP2C19&#x2a;2</i> alleles correlate with clopidogrel responsiveness following the administration of clopidogrel in healthy Malaysian volunteers. <i  >Methods</i>. Ninety volunteers were genotyped for <i  >CYP2C19&#x2a;2</i> and <i  >CYP2C19&#x2a;3</i> alleles. Forty-five of 90 volunteers were included in the clopidogrel response studies and triaged into three genotypes, namely, <i  >CYP2C19&#x2a;1/&#x2a;1 </i><svg     style="vertical-align:-2.3205pt;width:56.162498px;" id="M1" height="15.0875" version="1.1" viewBox="0 0 56.162498 15.0875" width="56.162498"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,12.138)"><path id="x28" d="M300 -147l-18 -23q-106 71 -159 185.5t-53 254.5v1q0 139 53 252.5t159 186.5l18 -24q-74 -62 -115.5 -173.5t-41.5 -242.5q0 -130 41.5 -242.5t115.5 -174.5z" /></g><g transform="matrix(.017,-0,0,-.017,5.944,12.138)"><path id="x1D45B" d="M495 86q-46 -47 -87 -72.5t-63 -25.5q-43 0 -16 107l49 210q7 34 8 50.5t-3 21t-13 4.5q-35 0 -109.5 -72.5t-115.5 -140.5q-21 -75 -38 -159q-50 -10 -76 -21l-6 8l84 340q8 35 -4 35q-17 0 -67 -46l-15 26q44 44 85.5 70.5t64.5 26.5q35 0 10 -103l-24 -98h2&#xA;q42 56 97 103.5t96 71.5q46 26 74 26q9 0 16 -2.5t14 -11.5t9.5 -24.5t-1 -44t-13.5 -68.5q-30 -117 -47 -200q-4 -19 -3.5 -25t6.5 -6q21 0 70 48z" /></g><g transform="matrix(.017,-0,0,-.017,19.186,12.138)"><path id="x3D" d="M535 323h-483v50h483v-50zM535 138h-483v50h483v-50z" /></g><g transform="matrix(.017,-0,0,-.017,33.89,12.138)"><path id="x31" d="M384 0h-275v27q67 5 81.5 18.5t14.5 68.5v385q0 38 -7.5 47.5t-40.5 10.5l-48 2v24q85 15 178 52v-521q0 -55 14.5 -68.5t82.5 -18.5v-27z" /></g><g transform="matrix(.017,-0,0,-.017,42.049,12.138)"><path id="x37" d="M447 623l8 -12l-283 -613l-74 -10l-7 11q174 283 297 551h-216q-48 0 -62.5 -12t-33.5 -63h-29q10 60 18 148h382z" /></g><g transform="matrix(.017,-0,0,-.017,50.209,12.138)"><path id="x29" d="M275 270q0 -296 -211 -440l-19 23q75 62 116.5 174t41.5 243t-42 243t-116 173l19 24q211 -144 211 -440z" /></g>

		
	
</svg>, <i  >CYP2C19&#x2a;1/&#x2a;2 </i><svg     style="vertical-align:-2.3205pt;width:60.037498px;" id="M2" height="15.0875" version="1.1" viewBox="0 0 60.037498 15.0875" width="60.037498"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,12.138)"><use xlink:href="#x28"/></g><g transform="matrix(.017,-0,0,-.017,5.944,12.138)"><use xlink:href="#x1D45B"/></g><g transform="matrix(.017,-0,0,-.017,19.186,12.138)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,33.89,12.138)"><path id="x32" d="M412 140l28 -9q0 -2 -35 -131h-373v23q112 112 161 170q59 70 92 127t33 115q0 63 -31 98t-86 35q-75 0 -137 -93l-22 20l57 81q55 59 135 59q69 0 118.5 -46.5t49.5 -122.5q0 -62 -29.5 -114t-102.5 -130l-141 -149h186q42 0 58.5 10.5t38.5 56.5z" /></g><g transform="matrix(.017,-0,0,-.017,42.049,12.138)"><use xlink:href="#x31"/></g><g transform="matrix(.017,-0,0,-.017,50.209,12.138)"><use xlink:href="#x29"/></g><g transform="matrix(.017,-0,0,-.017,56.09,12.138)"><path id="x2C" d="M95 130q31 0 61 -30t30 -78q0 -53 -38 -87.5t-93 -51.5l-11 29q77 31 77 85q0 26 -17.5 43t-44.5 24q-4 0 -8.5 6.5t-4.5 17.5q0 18 15 30t34 12z" /></g>

		
	
</svg> and <i  >CYP2C19&#x2a;2/&#x2a;2 </i><svg     style="vertical-align:-2.3205pt;width:48px;" id="M3" height="15.0875" version="1.1" viewBox="0 0 48 15.0875" width="48"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,12.138)"><use xlink:href="#x28"/></g><g transform="matrix(.017,-0,0,-.017,5.944,12.138)"><use xlink:href="#x1D45B"/></g><g transform="matrix(.017,-0,0,-.017,19.186,12.138)"><use xlink:href="#x3D"/></g><g transform="matrix(.017,-0,0,-.017,33.89,12.138)"><use xlink:href="#x37"/></g><g transform="matrix(.017,-0,0,-.017,42.049,12.138)"><use xlink:href="#x29"/></g>

		
	
</svg>. All subjects received 300&#x2009;mg of clopidogrel, and platelet reactivity was assessed after a four-hour loading utilizing the VerifyNow-P2Y12 assay. Platelet activity was reported using P2Y12 reaction units (PRUs), and nonresponder status was prespecified at PRU&#x2009;&#x2265;&#x2009;230. <i  >Results</i>. Following clopidogrel intake, <i  >CYP2C19&#x2a;2/&#x2a;2</i> carriers had a significantly higher mean PRU compared to the <i  >CYP2C19&#x2a;1/&#x2a;2</i> and <i  >CYP2C19&#x2a;1/&#x2a;1</i> (291.0 &#xb1; 62.1 versus 232.5 &#xb1; 81.4 versus 147.4 &#xb1; 87.2 PRU, <svg     style="vertical-align:-0.1638pt;width:66.875px;" id="M4" height="11.375" version="1.1" viewBox="0 0 66.875 11.375" width="66.875"  xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg">
	
		
			<g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x1D443" d="M619 482q0 -69 -40.5 -119t-96 -72.5t-118.5 -26.5h-44l-70 20l-31 -151q-14 -67 0.5 -83t89.5 -22l-5 -28h-287l8 28q65 7 81.5 22t29.5 83l79 398q12 56 0.5 70.5t-78.5 20.5l7 28h255q108 0 164 -43t56 -125zM524 478q0 141 -146 141q-25 0 -47 -8q-16 -6 -20.5 -13.5&#xA;t-10.5 -39.5l-43 -241q37 -13 83 -13q67 0 125.5 45t58.5 129z" /></g><g transform="matrix(.017,-0,0,-.017,15.582,11.112)"><path id="x3C" d="M512 -3l-437 233v51l437 233v-58l-378 -200v-2l378 -199v-58z" /></g><g transform="matrix(.017,-0,0,-.017,30.286,11.112)"><path id="x30" d="M241 635q53 0 94 -28.5t63.5 -76t33.5 -102.5t11 -116q0 -58 -11 -112.5t-34 -103.5t-63.5 -78.5t-94.5 -29.5t-95 28t-64.5 75t-34.5 102.5t-11 118.5q0 58 11.5 112.5t34.5 103t64.5 78t95.5 29.5zM238 602q-32 0 -55.5 -25t-35.5 -68t-17.5 -91t-5.5 -105&#xA;q0 -76 10 -138.5t37 -107.5t69 -45q32 0 55.5 25t35.5 68.5t17.5 91.5t5.5 105t-5.5 105.5t-18 92t-36 68t-56.5 24.5z" /></g><g transform="matrix(.017,-0,0,-.017,38.446,11.112)"><path id="x2E" d="M113 -12q-24 0 -39.5 16t-15.5 42q0 24 16 40.5t40 16.5t40 -16.5t16 -40.5q0 -26 -16 -42t-41 -16z" /></g><g transform="matrix(.017,-0,0,-.017,42.321,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,50.481,11.112)"><use xlink:href="#x30"/></g><g transform="matrix(.017,-0,0,-.017,58.64,11.112)"><use xlink:href="#x31"/></g>

		
	
</svg>) carriers. Almost half of the participants (46.7&#x25;) were found to be nonresponders (3 were <i  >CYP2C19&#x2a;1/&#x2a;1</i>, 11 were <i  >CYP2C19&#x2a;1/&#x2a;2</i>, and 7 were <i  >CYP2C19&#x2a;2/&#x2a;2</i>). <i  >Conclusion</i>. In healthy Malaysian volunteers, <i  >CYP2C19&#x2a;2</i> allele was associated with a decrease in platelet responsiveness to clopidogrel. However, clopidogrel nonresponders can be found not only in the carriers of <i  >CYP2C19&#x2a;2/&#x2a;2</i>, but also in the carriers of <i  >CYP2C19&#x2a;1/&#x2a;2</i> and <i  >CYP2C19&#x2a;1/&#x2a;1</i>. The present paper demonstrated that genotype information does not correlate with clopidogrel response, and genotyping may represent a less robust approach compared to platelet activity testing in guiding clopidogrel therapy.

Yanti Nasyuhana Sani

Lim Sheau Chin

Lim Luen Hui

Nur Elyana Yazmin Mohd Redhuan Shah Edwin

Goh Teck Hwa

Victor L. Serebruany

Yuen Kah Hay

The CYP2C19&#x2a;1/&#x2a;2 Genotype Does Not Adequately Predict Clopidogrel Response in Healthy Malaysian Volunteers

The incidence and prevalence of atrial fibrillation (AF) are projected to increase significantly worldwide, imposing a significant burden on healthcare resources. The disease itself is extremely heterogeneous in its epidemiology, pathophysiology, and treatment options based on individual patient characteristics. Whilst ageing is well recognised to be an independent risk factor for the development of AF, this condition also affects the young in whom the condition is frequently symptomatic and troublesome. Traditional thinking suggests that the causal factors and pathogenesis of the condition in the young with structurally normal atria but electrophysiological &#x201c;triggers&#x201d; in the form of pulmonary vein ectopics leading to lone AF are in stark contrast to that in the elderly who have AF primarily due to an abnormal substrate consisting of fibrosed and dilated atria acting in concert with the pulmonary vein triggers. However, there can be exceptions to this rule as there is increasing evidence of structural and electrophysiological abnormalities in the atrial substrate in young patients with &#x201c;lone AF,&#x201d; as well as elderly patients who present with idiopathic AF. These reports seem to be blurring the distinction in the pathophysiology of so-called idiopathic lone AF in the young versus that in the elderly. Moreover with availability of improved and modern investigational and diagnostic techniques, novel causes of AF are being reported thereby seemingly consigning the diagnosis of &#x201c;lone AF&#x201d; to a rather mythical existence. We shall also elucidate in this paper the differences seen in the epidemiology, causes, pathogenesis, and clinical features of AF in the young versus that seen in the elderly, thereby requiring clearly defined management strategies to tackle this arrhythmia and its associated consequences.

Rajiv Sankaranarayanan

Graeme Kirkwood

Katharine Dibb

Clifford J. Garratt

Comparison of Atrial Fibrillation in the Young versus That in the Elderly: A Review

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<p><em>Cardiology Research and Practice</em> publishes original research articles and&nbsp;review articles&nbsp;focusing on the diagnosis and treatment of cardiovascular diseases, including hypertension, arrhythmia, heart failure, and vascular disease.</p>


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<p>Dr. Terrence Ruddy is Director of Nuclear Cardiology at the University of Ottawa Heart Institute, and Professor of Medicine and Radiology at the University of Ottawa. His research is in SPECT and PET imaging techniques in cardiovascular disease.</p>


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Cardiology Research and Practice publishes original research articles and review articles focusing on the diagnosis and treatment of cardiovascular diseases, including hypertension, arrhythmia, heart failure, and vascular disease.

Cardiology Research and Practice