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Acute Coronary Syndrom

From Early Pharmacology to Recent Pharmacology Interventions in Acute Coronary Syndromes High-Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long-Term Outcomes Randomized trial of complete versus lesion-only revascularization in patients undergoing primary percutaneous coronary intervention for STEMI and multivessel disease: the CvLPRIT trial Long-Term Prognostic Implications of Previous Silent Myocardial Infarction in Patients Presenting With Acute Myocardial Infarction Complete revascularisation versus treatment of the culprit lesion only in patients with ST-segment elevation myocardial infarction and multivessel disease (DANAMI-3—PRIMULTI): an open-label, randomised controlled trial An open-Label, 2 × 2 factorial, randomized controlled trial to evaluate the safety of apixaban vs. vitamin K antagonist and aspirin vs. placebo in patients with atrial fibrillation and acute coronary syndrome and/or percutaneous coronary intervention: Rationale and design of the AUGUSTUS trial Contemporary Diagnosis and Management of Patients With Myocardial Infarction in the Absence of Obstructive Coronary Artery Disease: A Scientific Statement From the American Heart Association Single-Molecule hsTnI and Short-Term Risk in Stable Patients With Chest Pain Myocardial Infarction in Young Women Culprit versus multivessel coronary intervention in ST-segment elevation myocardial infarction: a meta-analysis of randomized trials

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JOURNAL：ACC Article Link

SCAI Clinical Expert Consensus Statement on Cardiogenic Shock

Vikas Aggarwal, MBBS, MPH , FACC

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The following are key points to remember from this summary of the Society for Cardiovascular Angiography and Interventions (SCAI) Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock (CS). The document is endorsed by the American College of Cardiology, American Heart Association, Society of Critical Care Medicine, and Society of Thoracic Surgeons:

A system describing stages of CS from “A to E” is proposed. The purpose of this proposed classification of CS is to enable clear communication regarding patient status and to allow clinical trials to appropriately differentiate CS patient subsets.

Stage A:Patient who is“at risk”for CS but is not experiencing signs or symptoms of CS (e.g., someone with non–ST-segment elevation myocardial infarction (NSTEMI). This patient is warm and perfusing, and has normal cardiac index and no sign of volume overload or hypoperfusion.
Stage B: “beginning”shock or compensated shock where a patient may be volume overloaded, tachycardic, and/or hypotensive but no evidence of hypoperfusion on physical exam or laboratory studies.
Stage C is“classic”CS: Stage B patient with evidence of hypoperfusion on physical exam and laboratory studies “Cold and Wet.” Invasive hemodynamics (if available) demonstrate the classic depressed cardiac index associated with CS.
Stage D is“deteriorating”: Stage C plus failure of initial interventions in restoring adequate perfusion in 30 minutes and further escalation is required. Escalation is an increase in the number or intensity of intravenous therapies to address hypoperfusion, or addition of mechanical circulatory support after the initial 30-minute period of observation and treatment.
Stage E is“extremis”: Patient is highly unstable, often with circulatory collapse and/or refractory cardiac arrest with ongoing cardiopulmonary resuscitation (CPR). They are being supported by multiple simultaneous acute interventions including extracorporeal membrane oxygenation (ECMO)-facilitated CPR (eCPR).

Additionally, the(A)modifier for cardiac arrest is applied to describe those who suffer a cardiac arrest irrespective of duration (treated with chest compressions or direct current cardioversion). Accordingly, a patient may be in stage B_A shock, indicating stage B with a cardiac arrest complicating the clinical picture (e.g., a patient who presents with ventricular fibrillation in the setting of acute MI and rapidly stabilizes with prompt defibrillation).

Other key points highlighted are:

Troponin T is an independent prognostic indicator of adverse outcomes and can be used as a patient risk-stratifying tool. Elevation of troponin in CS may identify patients who present late.
Arterial lactate is preferable since venous lactate is generally higher than arterial lactate and the 2.0 mmol/L cut-off is best established for arterial lactate.
A low serum bicarbonate level is a better predictor of 30-day mortality than the highest recorded lactate level.
A low B-type natriuretic peptide (BNP) level argues against CS in the setting of hypotension; however, an elevated BNP level does not establish the diagnosis, as any form of cardiac ventricular or atrial stress may elevate levels of this peptide.
It is recommended to use a pulmonary artery catheter in the diagnosis and management of CS patients, along with rapidly transferring those requiring a higher level of care to an experienced shock center.
Mixed shock patients have features suggestive of systemic inflammation, with or without proven infection. Such systemic vasodilation exacerbates systemic hypoperfusion and decreases coronary perfusion pressure. The potential for mixed shock emphasizes the importance of invasive hemodynamic monitoring.

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SCAI Clinical Expert Consensus Statement on Cardiogenic Shock

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