Name: intracoronary acetylcholine provocation testing for assessment of coronary vasomotor disorders
Uploaded: 2016-08-18T14:00:00.000+00:00
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Description: Watch this Scientific Journal Video about Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders at JoVE.com

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NOT: İntrakoroner asetilkolin testi yerel etik kurul tarafından onaylandı ve protokol insan araştırma için kurumumuzun yönergeleri takip eder. Asetilkolin Çözümleri 1. Hazırlama (Malzeme Tablosu bakınız) <ol><li> paketi ile sağlanan çözücü 2 ml 20 mg asetilkolin karıştırın. </li><li> NaCl% 0.9 98 ml 2 mi ACH solüsyonu eklenir. Bu mi 0.2 mg / bir doza karşılık gelir ve NaCl 91 ml% 0.9 stok çözeltisi 1 9 ml ekleyin stok çözeltisi 1 olarak adlandırılan, bu mi 18 ug / bir doza karşılık gelir ve stok solüsyon 2 olarak adlandırılır. </li><li> , &quot;Yüksek&quot;, &quot;orta&quot; ve &quot;düşük&quot; olarak etiketlenmiş 3 perfüzyon şırınga (50 ml her biri) hazırlayın. stok solüsyonu 2 40 ml &quot;yüksek&quot; etiketli perfüzyon şırınga 1 doldurun. </li><li> perfüzyon şırınga (yüksek) 1 8 ml perfüzyon şırınga 2 (etiketli &quot;orta&quot;) doldurun ve 0.9 NaCl 32 ml% ekleyin. Bu tekabül3.6 ug / ml dozu. </li><li> Perfüzyon şırınga 3 doldurun perfüzyon şırınga 2 (orta) 4 ml ( &quot;düşük&quot; etiketli) ve% 0.9 NaCI 36 ilave edin. Bu 0.36 ug / ml &#39;lik bir doza karşılık gelir. </li></ol> Asetikolinin İntrakoroner Enjeksiyon için Şırınga 2. Hazırlık <ol><li> intrakoroner enjeksiyon için 5 şırınga hazırlama (5 ml 4 şırınga [# 1, # 2, # 3, # 4] ve 10 ml 1 şırınga). </li><li> &quot;Düşük&quot; etiketli perfüzyon şırınga 6 ml 5 ml şırınga 1. doldurun (adım 1.5 bakınız). Bu, yaklaşık 2 ug bir doza karşılık gelir. </li><li> &quot;Orta&quot; etiketli perfüzyon şırınga 6 ml 5 ml şırınga 2. doldurun. Bu, yaklaşık 20 ug arasında bir doza karşılık gelir. </li><li> &quot;Yüksek&quot; etiketli perfüzyon şırınga 5.5 ml 5 ml şırınga 3. doldurun. Bu, yaklaşık 100 ug arasında bir doza karşılık gelir. </li><li> etiketli perfüzyon şırınga 11 ml, 10 ml şırınga doldurun4;. &quot;Yüksek Bu, yaklaşık 200 ug bir doza karşılık gelir. </li><li> &quot;Yüksek&quot; etiketli perfüzyon şırınga 4.5 ml 5 ml şırınga 4. doldurun. Bu, yaklaşık 80 ug, bir doza karşılık gelir. bir kenara bu şırıngayı koyun ve sadece sağ koroner arter değerlendirilmesi için kullanabilirsiniz. </li></ol> 3. Teşhis Koroner Anjiyografi <ol><li> lokal anestezi enjekte ya sağ radial arter yakınlığı (genellikle 2 mepivacain ml) ya da sağ femoral arter (mepivacain genellikle 15 ml) yakınlığı içinde. </li><li> Lokal anestezi başarısını onaylamak iğne ile anestezi-cilt batıcı ve ağrı hala mevcut olup olmadığını hastayı sorarak olduğunu. </li><li> Daha sonra kanül içinden tel takmak ve çıkarmak, bir kanül ile Seldinger tekniği 13 göre arter delinme. tel üzerinden kılıf (genellikle 5K) yerleştirin. steril koşullar altında koroner anjiyografi gerçekleştirin. </li><li> tel th Advancekaba çıkan aorta kılıf ve aort kapağının üstünde tanı kateter yerleştirin. Sonra teli çıkarın ve kontrast şırınga ile kateter bağlayın. NOT: kontrast maddesi iyomeprol, trometamol, hidroklorik asit ve su içerir. </li><li> hafif çekerek ve kateter çevirerek sol ana kök sol koroner arter için tanısal kateter yerleştirin. kontrast madde 2 ml enjekte edilerek kateterin doğru konumlandırılmasını onaylayın. </li><li> Farklı görünümlerde koroner arterleri görselleştirmek için kontrast yaklaşık 10 ml manuel enjeksiyonu ile Judkins tekniği 14&#39;e göre koroner anjiyografi gerçekleştirin. NOT: Genellikle LAO 40 ° ve 35 ° RAO sağ koroner arter için kullanılır ve LAO 45 ° / CRAN 25 °, RAO 30 ° / CRAN 30 ° ve 20 ° RAO / Caud 30 ° sol koroner arter için kullanılır. </li><li> (Ilgili herhangi bir epikardiyal darlık çıkarıldıktan sonra ≥50 asetilkolin testi başlatgörsel değerlendirme ile%). </li></ol> Asetikolinin 4. İntrakoroner Enjeksiyon <ol><li> Sol koroner artere 2 mikrogram şırınga içerisinde 1. 6 ml enjekte edilir. EKG ve hastanın semptomlarının (örneğin göğüs ağrısı, nefes darlığı, baş dönmesi) sürekli izlenmesi ile 20 sn içinde bu enjekte edilir. 6 ml enjeksiyondan sonra sol koroner arter (genellikle bir RAO 20 ° / Caud 30 ° projeksiyon iyi projeksiyonu) koroner anjiyografi gerçekleştirin. </li><li> elle kateter içine kontrast şırıngayla aksine 10 ml enjekte edilerek koroner anjiyografi gerçekleştirin. 12-kurşun-EKG kaydedildi ve asetilkolin her dozdan sonra basılmalıdır. 1 dakika duraklama her doz arasında olmalıdır. </li><li> Sol koroner artere 20 ug şırınga içerisinde 2. 6 ml enjekte edilir. Sürekli EKG izlenmesi ve hastanın semptomları olan 20 sn içinde bu enjekte edilir. enjeksiyondan sonra sol koroner arterin koroner anjiyografi gerçekleştirin6 ml yukarıda belirtildiği gibi. </li><li> Sol koroner artere 100 ug şırınga içerisinde 3. 5.5 ml enjekte edilir. Sürekli EKG izlenmesi ve hastanın semptomları olan 20 sn içinde bu enjekte edilir. Yukarıda belirtildiği gibi 5.5 ml enjekte edildikten sonra, sol koroner arterin koroner anjiografi gerçekleştirin. NOT: Çoğu hasta, bazı belirtiler rapor, bu dozda EKG değişiklikleri veya epikardiyal vazokonstriksiyona göstermektedir. Bazen manuel enjeksiyon hızı yavaşladı gerekiyor. ACH-testleri için farklı protokoller, aşağıda belirtildiği gibi, enjeksiyon farklı bir hız ile kullanılmaktadır. 20 saniye içinde, enjeksiyon ile karşılaştırıldığında 3 dakikalık bir süre boyunca yavaş bir enjeksiyonu da uygun olabilir. </li><li> Hiçbir spazm (200 mikrogram nitroglyercine enjeksiyonundan sonra geminin rahat durumuna göre yani&gt;% 90 vazokonstriksiyon) 100 mg dozda oluşursa 200 mikrogram (10 ml şırınga) ACH dozu ile devam ediyor. Sürekli monitör ile 20 saniye içinde 11 ml enjekte edilirEKG ve hastanın semptomlarının ing. </li><li> (Bölüm 3) yukarıda da belirtildiği gibi 11 ml enjeksiyonundan sonra sol koroner arterin koroner anjiyografi gerçekleştirin. Not: 200 ug doz birçok hastada uygulanmış olsa da intrakoroner asetilkolin uygun dozları tam olarak tanımlanmış olan kaldığı belirtilmelidir. Bazı yazarlar 100 ug sol koroner arter için maksimum doz olması gerektiğini göstermektedir. NOT: Genellikle bradikardi oluşur ve enjeksiyon hızı yavaşladı gerekiyor. </li><li> anormal bulgular sol koroner arterin test sırasında görülür ise sağ koroner artere 80 mikrogram ACH (4.5 ml, şırınga # 4) enjekte edilir. Sürekli EKG izlenmesi ve hastanın semptomları olan 20 sn içinde bu enjekte edilir. Genellikle bradikardi oluşur ve enjeksiyon hızı uzun süreli bradikardi ve / veya asistoli önlemek için yavaşladı gerekiyor. </li><li> sağ koroner arterin koroner anjiyografi gerçekleştirin4.5 ml (genellikle LAO 40 ° / 0 ° projeksiyon en iyisi) (bölüm 3) yukarıda da belirtildiği gibi enjeksiyonundan sonra. </li><li> Bir testten sonra her test artere 200 mikrogram doz veya şiddetli semptomlar (örneğin şiddetli göğüs ağrısı veya nefes darlığı ciddi), iskemik EKG değişimleri veya epikardiyal spazm meydana ile intrakoroner nitrogliserin enjekte edilir. </li><li> Görüntü spazm reversion belgelemek için bir dakika sonra adım 4.2 belirtildiği gibi gemi. </li></ol>

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The authors have nothing to disclose.

Kateterizasyon laboratuarında günlük klinik rutin asetilkolin testi uygulamak mümkündür. Dışında ACH çözümleri hazırlanmasından radyolusen EKG dahil Teste başlamadan sürekli 12-lead EKG kaydı için yol önce çözülmesi gereken birçok teknik sorunlar vardır. Bu test sırasında geçici iskemik EKG değişiklikleri tespit edebilmek için esastır. Ayrıca, ACH çözüm sadece 2 saat için kullanılabilir olduğunu bilmek önemlidir. Bundan sonra onlar yeni hazırlanmalıdır. <p class="jove_conten...

Angina pektoris, koroner arter hastalığının en belirgin özelliği ve uzun yıllar kurulmuştur miyokard iskemisi ve egzersize bağlı angina neden bir epikardiyal darlık kavramıdır. Ancak, angina pektoris ile birçok hasta nitrogliserin veya geri kalanı tarafından egzersiz ve rahatlama sırasında retrosternal ağrı, başlangıç ​​tipik üçlü yok. Sık hastalar olası bir angina eşdeğeri olarak emek üzerine anjin dinlenme veya efor ve dinlenme angina bir kombinasyonu olarak pektoris yanı sıra nefes darlığı rapor. 1959 yılında Prinzmetal elektrokardiyogram (EKG) ST segment yükselmesi ile ilişkili istirahatte anjina neden koroner arterlerin geçici spazm kavramını tanıtmak için ilk ama korunmuş egzersiz kapasitesi 1 oldu. Bu hipotez koroner anjiyografi ile daha sonra teyit ve koroner spazm epikardiyal darlıkları ya da normal koroner arterleri 2 olan hastalarda mevcut olabilir olduğu gözlendi. 1980i olarakes koroner arter spazmı tespiti için (ACH-testi) testi intrakoroner asetilkolin provokasyon Japonya&#39;da kurulmuş ve koroner spazm 3 artış için klinik araştırmalarda sonradan ilgi oldu. Ancak, 1977 yılında perkütan koroner girişim tanıtımı ve 1986 yılında ilk stent implantasyonu sonrası koroner vazomotor bozukluklar ilgi en azından Avrupa ve Amerika Birleşik Devletleri&#39;nde önemli ölçüde azalmıştır. (Nedeniyle, sadece koroner spazm değerlendirilmesi için, koroner arterlere uygulanabilir ACh kısa yarılanma ömrü) bağlı ACH-testi invaziv da olabilir. Yine, işaret ve miyokard iskemi semptomları olan birçok hastada koroner anjiyografi 4,5,6 ilgili herhangi epikardiyal darlık yoktur. Bu tür hastalarda intrakoroner asetilkolin provokasyon testi klinik olarak anlamlı koroner vazomotor bozukluk tespit ve uygun tıbbi tedaviye enstitü yararlıdır <sup&gt; 7. Asetilkolin parasempatik sinir sistemindeki bir nörotransmiterdir. Bu nikotinik hem de muscarinergic (mAChR) reseptörleri yoluyla göstermektedir. ikinci vaskular homeostaz için önemli olan ve asetilkolin, bir seçici olmayan agonist olarak mAChR ile bağlanır. Endotel düzeyinde Bu reseptörlerin aktivasyonu vazokonstriksiyon 8 neden vasküler düz kas hücreleri üzerindeki mAChR aktivasyonu ise nitrik oksit aracılı vazodilatasyona neden olur. endotel bütünlüğü ve düz kas hücrelerinin reaktivitesine bağlı olarak, intrakoroner asetilkolin tatbikat net etkisi vazodilatasyon ve vazokonstriksiyon olup. insan asetilkolin yanıt olarak koroner arterlerin fizyolojik tepki tam olarak anlaşılmış değildir ancak normal koroner arterleri ve hastalarda görüldüğü gibi damar çapının% 25&#39;e varan bir vazodilatasyon yanı sıra vazokonstriksiyon hiçbir fizyolojik olabileceği bildirilmiştir anjina pecToris 9. İntrakoroner asetilkolin provokasyon testi Kardiyoloji kılavuzların 10 European Society yanı sıra anjina pektoris ve engelsiz koroner arterleri olan hastalarda epikardiyal ve / veya mikrovasküler spazm değerlendirilmesi için Japon Yayma Cemiyeti kılavuzların 11 tarafından tavsiye edilmiştir. İntrakoroner asetilkolin provokasyon testi standart bir protokol 12 takip edilen 2006 yılından bu yana 2003 yılında kurumumuzun kateterizasyon laboratuvarında günlük klinik rutin kurulmuştur. ACH-testi genellikle koroner anjiyografide henüz belirti ve miyokard iskemi semptomları olan tüm hastalarda ilgili hiçbir epikardiyal darlık (&lt;% 50) yapılır. ACH-testi aşağıda tarif edilen protokole göre diagnostik koroner anjiyografi hemen sonra gerçekleştirilir. Ergonovin farklı bir etki mekanizmasına sahip spazmı provokasyon testi için kullanılan başka bir maddedir. Detaylıergonovin testi hakkında bilgi başka bir yerde 12 bulunabilir.

<table><tbody><tr><td>Vial of 20 mg acetylcholine chloride powder and 1 Ampoule of 2 ml diluent</td><td>Bausch &amp;amp; Lomb&amp;nbsp;</td><td>NDC 24 208-539-20</td><td></td></tr><tr><td>3x 100 ml NaCl 0.9 %</td><td>BBraun</td><td>3200950</td><td></td></tr><tr><td>3x syringe 50 ml each</td><td>BBraun</td><td>4187903</td><td></td></tr><tr><td>1x 2 ml syringe</td><td>BBraun</td><td>4606027V</td><td></td></tr><tr><td>1x 10 ml syringe</td><td>BBraun</td><td>4606108V</td><td></td></tr><tr><td>2x cannula 20 G 70 mm</td><td>BBraun</td><td>4665791</td><td></td></tr><tr><td>5x 5 ml syringe</td><td>BBraun</td><td>4606051V</td><td></td></tr><tr><td>Contrast agent Imeron 350 with a 10 ml syringe for contrast injection</td><td>Bracco Imaging</td><td>30699.03.00</td><td></td></tr><tr><td>Coronary angiography suite (AXIOM Artis MP eco )</td><td>Siemens</td><td>n/a</td><td></td></tr></tbody></table>

intracoronary acetylcholine provocation testing for assessment of coronary vasomotor disorders

Intracoronary acetylcholine provocation testing (ACH-test) is an established method for assessment of epicardial coronary artery spasm in the catheterization laboratory which was introduced more than 30 years ago. Due to the short half-life of acetylcholine it can only be applied directly into the coronary arteries. Several studies have demonstrated the safety and clinical usefulness of this test. However, acetylcholine testing is only rarely applied in the U.S. or Europe. Nevertheless, it has been shown that 62% of Caucasian patients with stable angina and unobstructed coronary arteries on coronary angiography suffer from coronary vasomotor disorders that can be diagnosed with acetylcholine testing. In recent years it has been appreciated that the ACH-test not only assesses the presence of epicardial spasm but that it can also be useful for the detection of coronary microvascular spam. In such cases no epicardial spasm is seen after injection of acetylcholine but ischemic ECG shifts are present together with a reproduction of the patient's symptoms during the test. This article describes the experience with the ACH-test and its implementation in daily clinical routine.

asetilkolin testinin yorumlanması üç kritere dayanmaktadır. İlk olarak, hasta olsun veya olmasın belirtiler oluşabilir test boyunca istenir. Sık sık, hastalar göğüs ağrısı, nefes darlığı veya diğer belirtiler darlığı gibi her zamanki semptomların üreme rapor. Bu testin genel yorumlanması için önemli bir noktayı temsil eder. İkinci olarak, 12-kurşun-EKG kaydı sürekli böyle ST-segment depresyonu, ST-segment yükselmesi ve T-dalga alternans olarak iskemik EK...

Watch this Scientific Journal Video about Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders at JoVE.com

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

Intracoronary acetylcholine testing has been established for the assessment of epicardial coronary spasm more than 30 years ago. Recently, the focus has shifted towards the microcirculation and it has been shown that microvascular spasm can be detected using ACH-testing. This article describes the ACH-test and its implementation in daily routine.

Değerlendirme Koroner of Vazomotor Bozukluklar için intrakoroner asetilkolin Provokasyon Testi

Intracoronary acetylcholine provocation testing (ACH-test) is an established method for assessment of epicardial coronary artery spasm in the ...

intracoronary-acetylcholine-provocation-testing-for-assessment

Universidad de Cartagena UDEC

Research

JoVE Journal

Medicine

15.6K Görüntüleme.  Robert-Bosch-Krankenhaus. Intracoronary acetylcholine testing has been established for the assessment of epicardial coronary spasm more than 30 years ago. Recently, the focus has shifted towards the microcirculation and it has been shown that microvascular spasm can be detected using ACH-testing. This article describes the ACH-test and its implementation in daily routine.

Video: Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders

A Protocol for Comprehensive Assessment of Bulbar Dysfunction in Amyotrophic Lateral Sclerosis (ALS)

Improved methods for assessing bulbar impairment are necessary for expediting diagnosis of bulbar dysfunction in ALS, for predicting disease progression across speech subsystems, and for addressing the critical need for sensitive outcome measures for ongoing experimental treatment trials. To address this need, we are obtaining longitudinal profiles of bulbar impairment in 100 individuals based on a comprehensive instrumentation-based assessment that yield objective measures. Using instrumental approaches to quantify speech-related behaviors is very important in a field that has primarily relied on subjective, auditory-perceptual forms of speech assessment1. Our assessment protocol measures performance across all of the speech subsystems, which include respiratory, phonatory (laryngeal), resonatory (velopharyngeal), and articulatory. The articulatory subsystem is divided into the facial components (jaw and lip), and the tongue. Prior research has suggested that each speech subsystem responds differently to neurological diseases such as ALS. The current protocol is designed to test the performance of each speech subsystem as independently from other subsystems as possible. The speech subsystems are evaluated in the context of more global changes to speech performance. These speech system level variables include speaking rate and intelligibility of speech.
The protocol requires specialized instrumentation, and commercial and custom software. The respiratory, phonatory, and resonatory subsystems are evaluated using pressure-flow (aerodynamic) and acoustic methods. The articulatory subsystem is assessed using 3D motion tracking techniques. The objective measures that are used to quantify bulbar impairment have been well established in the speech literature and show sensitivity to changes in bulbar function with disease progression. The result of the assessment is a comprehensive, across-subsystem performance profile for each participant. The profile, when compared to the same measures obtained from healthy controls, is used for diagnostic purposes. Currently, we are testing the sensitivity and specificity of these measures for diagnosis of ALS and for predicting the rate of disease progression. In the long term, the more refined endophenotype of bulbar ALS derived from this work is expected to strengthen future efforts to identify the genetic loci of ALS and improve diagnostic and treatment specificity of the disease as a whole. The objective assessment that is demonstrated in this video may be used to assess a broad range of speech motor impairments, including those related to stroke, traumatic brain injury, multiple sclerosis, and Parkinson disease.

A Protocol for Comprehensive Assessment of Bulbar Dysfunction in Amyotrophic Lateral Sclerosis ALS

Objective assessments of the physiological mechanisms that support speech are needed to monitor disease onset and progression in persons with ALS and to quantify treatment effects in clinical trials. In this video, we present a comprehensive, instrumentation-based protocol for quantifying speech motor performance in clinical populations.

Amyotrophic Lateral Sclerosis bulber Disfonksiyon Kapsamlı Değerlendirmesi (ALS) için Protokol

Improved methods for assessing bulbar impairment are necessary for expediting diagnosis of bulbar dysfunction in ALS, for predicting disease progression ...

Tıp

Use of a Hanging Weight System for Coronary Artery Occlusion in Mice

Murine studies of acute injury are an area of intense investigation, as knockout mice for different genes are becoming increasingly available 1-38. Cardioprotection by ischemic preconditioning (IP) remains an area of intense investigation. To further elucidate its molecular basis, the use of knockout mouse studies is particularly important 7, 14, 30, 39. Despite the fact that previous studies have already successfully performed cardiac ischemia and reperfusion in mice, this model is technically very challenging. Particularly, visual identification of the coronary artery, placement of the suture around the vessel and coronary occlusion by tying off the vessel with a supported knot is technically difficult. In addition, re-opening the knot for intermittent reperfusion of the coronary artery during IP without causing surgical trauma adds additional challenge. Moreover, if the knot is not tied down strong enough, inadvertent reperfusion due to imperfect occlusion of the coronary may affect the results. In fact, this can easily occur due to the movement of the beating heart.
Based on potential problems associated with using a knotted coronary occlusion system, we adopted a previously published model of chronic cardiomyopathy based on a hanging weight system for intermittent coronary artery occlusion during IP 39. In fact, coronary artery occlusion can thus be achieved without having to occlude the coronary by a knot. Moreover, reperfusion of the vessel can be easily achieved by supporting the hanging weights which are in a remote localization from cardiac tissues.
We tested this system systematically, including variation of ischemia and reperfusion times, preconditioning regiments, body temperature and genetic backgrounds39. In addition to infarct staining, we tested cardiac troponin I (cTnI)
as a marker of myocardial infarction in this model. In fact, plasma levels of cTnI correlated with infarct sizes (R2=0.8). Finally, we could show in several studies that this technique yields highly reproducible infarct sizes during murine IP and myocardial infarction6, 8, 30, 40, 41. Therefore, this technique may be helpful for researchers who pursue molecular mechanisms involved in cardioprotection by IP using a genetic approach in mice with targeted gene deletion. Further studies on cardiac IP using transgenic mice may consider this technique.

A murine model for myocardial ischemia and ischemic preconditioning is an important tool study cardioprotective mechanisms in vivo. Here, we report an easy applicable in situ model for cardiac IP using a hanging-weight system for coronary artery occlusion.

Asma Ağırlık Sistemi Fare Koroner Arter Tıkanıklığı için kullanın

Murine studies of acute injury are an area of intense investigation, as knockout mice for different genes are becoming increasingly available 1-38. ...

Quantification of Absolute Myocardial Flow and Resistance by Continuous Thermodilution in Patients with Ischemia and Nonobstructive Coronary Artery Disease (INOCA)

In approximately half of the patients undergoing coronary angiography for angina pectoris or for signs or symptoms suggestive of ischemic heart disease, no obstructive coronary artery disease is angiographically visible. The majority of these patients with angina or ischemia and no obstructive coronary artery disease (INOCA) have an underlying coronary vasomotor dysfunction, and current consensus documents recommend diagnostic invasive coronary vasomotor function testing (CFT). 
During CFT, a variety of vasomotor dysfunction endotypes can be assessed, including vasospastic coronary dysfunction (epicardial or microvascular vasospasm), and/or microvascular vasodilatory dysfunction, including impaired vasodilatory capacity and increased microvascular resistance. The quantification of the continuous thermodilution derived absolute coronary blood flow and resistance might be a better measure compared to the currently used standard physiologic measures. This article provides an overview of this continuous thermodilution method.

Quantification of Absolute Myocardial Flow and Resistance by Continuous Thermodilution in Patients with Ischemia and Nonobstructive Coronary Artery Disease INOCA

Presented here is a protocol to measure absolute myocardial flow and resistance using continuous thermodilution in patients with ischemia and nonobstructive coronary artery disease.

In approximately half of the patients undergoing coronary angiography for angina pectoris or for signs or symptoms suggestive of ischemic heart disease, ...

Testing Acetylcholine Followed by Adenosine for Invasive Diagnosis of Coronary Vasomotor Disorders

More than 50% of patients with signs and symptoms of myocardial ischemia undergoing coronary angiography have unobstructed coronary arteries. Coronary vasomotor disorders (impaired vasodilatation and/or enhanced vasoconstriction/spasm) represent important functional causes for such a clinical presentation. Although impaired vasodilatation may be assessed with non-invasive techniques such as positron emission tomography or cardiac magnetic resonance imaging, there is currently no reliable non-invasive technique for the diagnosis of coronary spasm available. Thus, invasive diagnostic procedures (IDP) have been developed for the diagnosis of coronary vasomotor disorders including spasm testing as well as assessment of coronary vasodilatation. The identification of the underlying type of disorder (so called endotype) allows the initiation of targeted pharmacological treatments. Despite the fact that such an approach is recommended by the current European Society of Cardiology guidelines for the management of chronic coronary syndromes based on the CorMicA study, comparability of results as well as multicenter trials are currently hampered by major differences in institutional protocols for coronary functional testing. This article describes a comprehensive IDP protocol including intracoronary acetylcholine provocation testing for diagnosis of epicardial/microvascular spasm, followed by Doppler wire-based assessment of coronary flow reserve (CFR) and hyperemic microvascular resistance (HMR) in search of coronary vasodilatory impairment.

Coronary vasomotion disorders represent frequent functional causes of angina in patients with unobstructed coronaries. The underlying mechanism of angina (endotype) in these patients can be determined by a comprehensive invasive diagnostic procedure based on acetylcholine provocation testing followed by Doppler-derived assessment of the coronary flow reserve and microvascular resistance.

Koroner Vazomotor Bozuklukların İnvaziv Tanısı için Asetilkolin ve Adenozin Testi

More than 50% of patients with signs and symptoms of myocardial ischemia undergoing coronary angiography have unobstructed coronary arteries. Coronary ...

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function

Approximately 40% of patients undergoing invasive coronary angiography for investigation of angina are found to have no obstructive coronary artery disease (ANOCA). Abnormal coronary function underlies coronary vasomotion syndromes including coronary endothelial dysfunction, microvascular angina, vasospastic angina, post-PCI angina and myocardial infarction with no obstructive coronary arteries (MINOCA). Each of these endotypes are distinct subgroups, characterized by specific disease mechanisms. Diagnostic criteria and linked therapy for these conditions are now established by expert consensus and clinical guidelines.
Coronary function tests are performed as an adjunctive interventional diagnostic procedure (IDP) in appropriately selected patients during coronary angiography. This aids differentiation of patients according to endotype. The IDP includes two distinct components: a diagnostic guidewire test and a pharmacological coronary reactivity test. The tests last approximately 5 minutes for the former and 10-15 minutes for the latter. Patient safety and staff education are key.
The diagnostic guidewire test measures parameters of coronary flow limitation (fractional flow reserve [FFR], coronary flow reserve [CFR], microvascular resistance [index of microvascular resistance (IMR)], basal resistance index, and vasodilator function [CFR, resistive reserve ratio (RRR)]).
The pharmacological coronary reactivity test measures the vasodilator potential and propensity to vasospasm of both the main coronary arteries and the micro-vessels. It involves intra-coronary infusion of acetylcholine and glyceryl trinitrate (GTN). Acetylcholine is not licensed for parenteral use and is therefore prescribed on a named-patient basis. Vasodilatation is the normal, expected response to infusion of physiological concentrations of acetylcholine. Vascular spasm represents an abnormal response, which supports the diagnosis of vasospastic angina.
The purpose of this practical guide is to provide information on the preparation and administration of the IDP in clinical practice. It discusses some key preparation and safety considerations, as well as tips for procedural success. The IDP supports stratified medicine for a personalized approach to health and wellbeing.

The purpose of this practical guide is to provide information on the preparation and administration of an interventional diagnostic procedure in clinical practice. It discusses some key preparation and safety considerations, as well as tips for procedural success.

Girişimsel Tanı Prosedürü: Koroner Vasküler Fonksiyonun Değerlendirilmesi İçin Pratik Bir Kılavuz

Approximately 40% of patients undergoing invasive coronary angiography for investigation of angina are found to have no obstructive coronary artery ...

Acetylcholine Re-Challenge After Intracoronary Nitroglycerine Administration

Coronary artery spasm (CAS) can be diagnosed in a large proportion of patients with recurrent angina with non-obstructive coronary artery disease (ANOCA) using acetylcholine (ACh) spasm provocation testing. CAS can further be divided into different subtypes (e.g., focal, diffuse epicardial, or microvascular spasm), each with different pathophysiological mechanisms that may require tailored drug treatment. The evidence behind the role of nitrates in the setting of each CAS subtype is lacking, and the effectivity can vary on a per-patient basis. In order to assess on a per-patient level whether nitroglycerine (NTG) can prevent inducible spasm, the vasospastic ACh dose can be readministered after NTG administration as part of the spasm provocation test. The preventive effect of NTG is assessed by evaluating improvements in the severity of induced symptoms, ischemic ECG changes, and by reassessing the site and mode of spasm on angiography. This technique can therefore be used to assess the nitrate responsiveness on a per-patient level and unmask co-existing microvascular spasm in patients with epicardial spasm that is prevented with NTG. The NTG rechallenge, therefore, allows to further guide targeted therapy for CAS and provide new insights into the pathophysiological mechanism behind vasospastic disorders.

This protocol presents the acetylcholine rechallenge after nitroglycerine as an add-on procedure to spasm provocation testing. The purpose of this technique is to unmask co-existing microvascular spasm&#160;in patients with epicardial spasm&#160;and to assess the protective efficacy of nitroglycerine on a per-patient level to guide medical therapy.

İntrakoroner Nitrogliserin Uygulamasından Sonra Asetilkolin Yeniden Zorlanması

Coronary artery spasm (CAS) can be diagnosed in a large proportion of patients with recurrent angina with non-obstructive coronary artery disease (ANOCA) ...

Measurement of Myocardial Lactate Production for Diagnosis of Coronary Microvascular Spasm

In about a quarter of patients with angina and non-obstructive coronary arteries, no epicardial spasm is noted on coronary arteriography during an angina attack. Since the pressure-rate product is almost identical at rest and the onset of attack in those patients, the decrease in coronary blood flow rather than increased myocardial oxygen consumption is likely to explain myocardial ischemia, indicating a substantial involvement with coronary microvascular spasm (MVS). Myocardial lactate production, which could be defined as a negative myocardial lactate extraction ratio (ratio of the coronary arterial-venous difference in lactate concentration to arterial concentration), is considered indicative of objective evidence to support the emerging myocardial ischemia. Thus, monitoring of the myocardial lactate production and the emergence of chest pain and ischemic electrocardiographic changes during acetylcholine (ACh) provocation testing is of significant value for detecting the entity of MVS. Practically, 1 min after incremental doses of ACh (20, 50, and 100 &#956;g) are administered into the left coronary artery (LCA), paired samples of 1 mL of blood are collected from the LCA ostium and coronary sinus for measurement of lactate concentration by a calibrated automatic lactate analyzer. Then, the development of MVS could be confirmed by negative myocardial lactate extraction ratio despite the absence of angiographically demonstrable epicardial coronary spasm or before its occurrence throughout ACh provocation testing. In conclusion, assessment of myocardial lactate production is essential and valuable for the diagnosis of MVS.

Myocardial lactate production (coronary arterial-venous difference in serum lactate level) during coronary spasm provocation testing is considered as a highly sensitive marker that reflects acetylcholine-induced myocardial ischemia due to microvascular spasm. This article presents the procedures to assess myocardial lactate production for the diagnosis of coronary microvascular spasm.

Koroner mikrovasküler spazm tanısı için miyokardiyal laktat üretiminin ölçülmesi

In about a quarter of patients with angina and non-obstructive coronary arteries, no epicardial spasm is noted on coronary arteriography during an angina ...

Standardized Rat Coronary Ring Preparation and Real-Time Recording of Dynamic Tension Changes Along Vessel Diameter

As a key event of cardiovascular system diseases, coronary artery disease (CAD) has been widely regarded as the main culprit of atherosclerosis, myocardial infarction, and angina pectoris, which seriously threaten the life and health of people all over the world. However, how to record the dynamic biomechanical characteristics of isolated blood vessels has long puzzled people. Meanwhile, precise positioning and isolation of coronary arteries to measure in vitro dynamic vascular tension changes have become a trend in CAD drug development. The present protocol describes the macroscopic identification and microscopic separation of rat coronary arteries. The contraction and dilation function of the coronary artery ring along the vessel diameter was monitored using the established multi myograph system. The standardized and programmed protocols of coronary ring tension measurement, from sampling to data acquisition, tremendously improve the repeatability of the experimental data, which ensures the authenticity of vascular tension records after physiological, pathological, and drug intervention.

The present protocol describes the wire myograph technique for measuring vascular reactivity of the rat coronary artery.

Standartlaştırılmış Sıçan Koroner Halka Hazırlama ve Damar Çapı Boyunca Dinamik Gerilim Değişikliklerinin Gerçek Zamanlı Kaydı

As a key event of cardiovascular system diseases, coronary artery disease (CAD) has been widely regarded as the main culprit of atherosclerosis, ...

Oxygenation-sensitive Cardiac MRI with Vasoactive Breathing Maneuvers for the Non-invasive Assessment of Coronary Microvascular Dysfunction

Oxygenation-sensitive cardiac magnetic resonance imaging (OS-CMR) is a diagnostic technique that uses the inherent paramagnetic properties of deoxyhemoglobin as an endogenous source of tissue contrast. Used in combination with standardized vasoactive breathing maneuvers (hyperventilation and apnea) as a potent non-pharmacologic vasomotor stimulus, OS-CMR can monitor changes in myocardial oxygenation. Quantifying such changes during the cardiac cycle and throughout vasoactive maneuvers can provide markers for coronary macro- and microvascular function and thereby circumvent the need for any extrinsic, intravenous contrast or pharmacologic stress agents.
OS-CMR uses the well-known sensitivity of T2*-weighted images to blood oxygenation. Oxygenation-sensitive images can be acquired on any cardiac MRI scanner using a modified standard clinical steady-state free precession (SSFP) cine sequence, making this technique vendor-agnostic and easily implemented. As a vasoactive breathing maneuver, we apply a 4-min breathing protocol of 120 s of free breathing, 60 s of paced hyperventilation, followed by an expiratory breath-hold of at least 30 s. The regional and global response of myocardial tissue oxygenation to this maneuver can be assessed by tracking the signal intensity change. The change over the initial 30 s of the post-hyperventilation breath-hold, referred to as the breathing-induced myocardial oxygenation reserve (B-MORE) has been studied in healthy people and various pathologies. A detailed protocol for performing oxygen-sensitive CMR scans with vasoactive maneuvers is provided.
As demonstrated in patients with microvascular dysfunction in yet incompletely understood conditions, such as inducible ischemia with no obstructive coronary artery stenosis (INOCA), heart failure with preserved ejection fraction (HFpEF), or microvascular dysfunction after heart transplantation, this approach provides unique, clinically important, and complementary information on coronary vascular function.

The assessment of microvascular function by oxygenation-sensitive cardiac magnetic resonance imaging in combination with vasoactive breathing maneuvers is unique in its ability to assess rapid dynamic changes in myocardial oxygenation in vivo and, thus, may serve as a critically important diagnostic technique for coronary vascular function.

Koroner Mikrovasküler Disfonksiyonun Non-invaziv Değerlendirmesi için Vazoaktif Solunum Manevraları ile Oksijenasyona Duyarlı Kardiyak MRG

Oxygenation-sensitive cardiac magnetic resonance imaging (OS-CMR) is a diagnostic technique that uses the inherent paramagnetic properties of ...

Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues

Altered vascular tone responsiveness to pathophysiological stimuli contributes to the development of a wide range of cardiovascular and metabolic diseases. Endothelial dysfunction represents a major culprit for the reduced vasodilatation and enhanced vasoconstriction of arteries. Adipose (fat) tissues surrounding the arteries play important roles in the regulation of endothelium-dependent relaxation and/or contraction of the vascular smooth muscle cells. The cross-talks between the endothelium and perivascular adipose tissues can be assessed ex vivo using mounted blood vessels by a wire myography system. However, optimal settings should be established for arteries derived from animals of different species, ages, genetic backgrounds and/or pathophysiological conditions.

The protocol describes the use of wire myography to evaluate the transmural isometric tension of mesenteric arteries isolated from mice, with special consideration of the modulation by factors released from endothelial cells and perivascular adipose tissues.