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Chest Pain Atypical Syndrome clinical trials

View clinical trials related to Chest Pain Atypical Syndrome.

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NCT ID: NCT02581540 Completed - Clinical trials for Cardiovascular Diseases

Mersey Acute Coronary Syndrome Rule-Out Using High Sensitive Troponin

MACROS
Start date: June 2011
Phase:
Study type: Observational

The aim of this observational study is twofold. The primary hypothesis being tested is that initial(first) high sensitivity Tn <5ng/l (limit of detection) combined with an ECG with no ischaemic changes is superior as an accelerated diagnostic tool/strategy compared to TIMI score (<2), GRACE <75 and HEART score ≤ 3. (Hs tn T- Roche elecsys HS tn T) and also against HS troponin at the 99th percentile (<15ng/l with nonischaemic changes)- again all scored with initial (first tn ) only. The second aim is to directly compare the three established methods of risk stratifying patients (predicting risk in suspected heart attacks) namely, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI) and HEART score in the era of high sensitivity troponins performs best.

NCT ID: NCT02056964 Completed - Clinical trials for Acute Coronary Syndrome

HEART Pathway Implementation

Start date: November 2013
Phase:
Study type: Observational

The purpose of this study is to determine the effectiveness of the HEART Pathway, a clinical decision aid for the care of patients with chest pain, in a "real-world" clinical setting. This will be accomplished through the building of a transformative collaboration between research, education, and health systems operations to more effectively and efficiently provide patient care.

NCT ID: NCT01839058 Completed - Clinical trials for Chest Pain Atypical Syndrome

Is Non-Cardiac Chest Pain Caused by Sustained Longitudinal Smooth Muscle Contraction?

Start date: October 2013
Phase:
Study type: Observational

Non-cardiac chest pain (NCCP) is a common disorder whose pathophysiology is poorly understood. Some evidence suggests it may be related to sustained esophageal contractions (SECs) of longitudinal smooth muscle. The investigators have previously shown that acid is a trigger for SECs and results in shortening of the esophagus. In this study, the investigators plan to prospectively evaluate esophageal shortening responses to acid in a group of patients with NCCP compared to controls. The investigators will use high resolution esophageal manometry coupled with acid infusion to evaluate shortening. The investigators hypothesize that at least a subset of patients with NCCP will have an exaggerated esophageal shortening response to acid which correlates with symptom production. If our hypothesis proves true, this may lead to a future therapeutic target in the treatment of these patients.