How to Pass the FRACP Written Examination. Jonathan Gleadle

Чтение книги онлайн.

Читать онлайн книгу How to Pass the FRACP Written Examination - Jonathan Gleadle страница 24

How to Pass the FRACP Written Examination - Jonathan  Gleadle

Скачать книгу

(ACS), but is elevated in many patients without ACS.

      Conditions associated with non‐ACS cTn elevations include:

       Tachyarrhythmias

       Congestive heart failure

       Malignant hypertension

       Sepsis

       Myocarditis

       Valvular heart disease (aortic stenosis)

       Aortic dissection

       Pulmonary embolism, pulmonary hypertension

       Chronic kidney disease

       Acute ischaemic or haemorrhagic stroke

       Cardiac contusion or cardiac procedures (CABG, PCI, ablation, pacing, cardioversion, or endomyocardial biopsy)

       Infiltrative diseases (amyloidosis, hemochromatosis, sarcoidosis)

       Myocardial drug toxicity or poisoning (doxorubicin, trastuzumab, snake venoms)

       Rhabdomyolysis.

      As cTn can be detected among healthy adults, there are guidelines regarding what is considered an ‘elevated’ level. The joint European/American College of Cardiology guidelines define a clinically relevant increase in cTn levels as a level that exceeds the 99th percentile of a normal reference population. However, using a statistical cut‐off means that some normal individuals will have a value above this cut‐off, and because other clinical causes can cause an elevation, cTn should be interpreted in the context of pre‐test probability of ACS. cTn concentrations are elevated in one in eight patients in the emergency department (ED).

      High‐sensitivity assays can accurately detect cTn at lower levels than older‐generation assays, giving them higher sensitivity for the detection of ACS at presentation, which means that the time interval to the second measurement of high‐sensitivity cTn (hs‐cTn) can be significantly shortened, thereby reducing the time to diagnosis and improving efficiency in the ED. There is concern that hs‐cTn may have lower diagnostic accuracy in patients with low pre‐test probability for ACS. Concern of misinterpretation of these hs‐cTn elevations as ACS and patient harm associated with potential unnecessary therapies such as anticoagulation and coronary angiography has led some experts to recommend withholding hs‐cTn testing in patients with a low pre‐test probability for ACS.

      However, practice guidelines also highlight that ACS frequently presents with atypical symptoms especially in the elderly and patients with diabetes. It recommends scrutiny for ACS with ECG and hs‐cTn. These divergent recommendations result in uncertainty in clinical practice regarding hs‐cTn testing in patients with low pre‐test probability for ACS. A recent retrospective analysis reported low specificity for hs‐cTn to diagnose MI when grouping ED patients with suspected MI together with patients with acute heart failure and patients with documented PE. Hence, it is very important to highlight that diagnostic testing with hs‐cTn should be applied to the correct population, at the optimal time and in the appropriate clinical context. This patient has very low pretest probability because her epigastric discomfort is nonspecific; her renal function is normal, and there are no other cardiovascular risk factors.

An illustration of the Quick Response code.

      Twerenbold R, Boeddinghaus J, Nestelberger T, Wildi K, Rubini Gimenez M, Badertscher P et al. Ref: JACC 70(8):996–1012.

      Clinical Use of High‐Sensitivity Cardiac Troponin in Patients With Suspected Myocardial Infarction. Twerenbold et al.

      2017;70(8):996–1012.

       https://pubmed.ncbi.nlm.nih.gov/28818210/

       35. Answer: B

      This elderly woman is septic due to severe pneumonia. She has multiple cardiovascular risk factors. Her ECG shows ischaemic change, and the troponin level is elevated. This is a typical case of type 2 myocardial infarction (MI).

      MI can be classified into various types, based on pathological, clinical, and prognostic differences, along with different treatment strategies:

       Type 1: Spontaneous myocardial infarction

      Spontaneous MI related to atherosclerotic plaque rupture, ulceration, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe coronary artery disease (CAD) but on occasion non‐obstructive or no CAD.

      In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g. coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy‐/brady‐arrhythmias, anaemia, respiratory failure, hypotension.

       Type 3: Myocardial infarction resulting in death when biomarker values are unavailable.

       Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI).

       Type 4b: Myocardial infarction related to stent thrombosis.

       Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG).

      Patients with type 2 MI are frequently encountered in clinical practice and may be more common than type 1 MI. Diagnostic criteria for type 2 MI include:

      Detection of a rise and/or fall of troponin values with at least one value above the 99th percentile, and evidence of an imbalance between myocardial oxygen supply and demand unrelated to acute coronary atherothrombosis, requiring at least one of the following:

       Symptoms of acute myocardial ischaemia

       New ischaemic ECG changes

       Development of pathological Q waves

       Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology.

      The diagnosis of type 2 MI is associated with a poor prognosis: less than 40% of patients will live 5 years past their diagnosis. In contrast, 65% of patients with type 1 MI will survive for 5 years. This is because type 2 MI typically occurs among older patients with multiple comorbidities and is identified in the context of hemodynamic instability, including shock, tachycardia, respiratory failure, gastrointestinal bleeding, decompensated heart failure, or recent surgery. Moreover, in contrast to type 1 MI that has a clear set of guideline‐based recommendations for treatment, management of type 2 MI remains uncertain.

      Although the benefits of antiplatelet agents, β‐blockers, and statins have been demonstrated among patients with type 1 MI, the utility of these medications among patients

Скачать книгу