PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock

Thiele, Holger; Akın, İbrahim; Sandri, Monica; Fuernau, Georg; Waha, Suzanne de; Meyer‐Saraei, Roza; Nordbeck, Peter; Geisler, Tobias; Landmesser, Ulf; Skurk, Carsten; Fach, Andreas; Lapp, Harald; Piek, Jan J.; Noč, Marko; Goslar, Tomaž; Felix, Stephan B.; Maier, Lars S.; Stępińska, Janina; Oldroyd, Keith G.; Šerpytis, Pranas; Montalescot, Gilles; Barthélémy, Olivier; Huber, Kurt; Windecker, Stephan; Savonitto, Stefano; Torremante, Patrizia; Vrints, Christiaan J.; Schneider, Steffen; Desch, Steffen; Zeymer, Uwe

doi:10.1056/nejmoa1710261

Cited by 854 publications

(640 citation statements)

References 26 publications

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“…Such data were not available in their current report [9]. Taking high dose statins before PCI (as compared to no statins or low dose statins) has been shown to reduce peri-PCI infarctions and 30-day events by ~50% in a metaanalysis of 13 studies with 3341 patients [10].…”

Section: Editorialmentioning

confidence: 78%

“…The CULPRIT-SHOCK findings serve to illustrate that PCI on stable noninfarct related lesions is not without its own risks [9]. The risk includes peri-PCI plaque embolization which may occur more frequently in patients without prior statin therapy.…”

Section: Editorialmentioning

confidence: 98%

Section: Editorialmentioning

confidence: 99%

“…In CULPRIT-SHOCK [9], 706 patients with multi-vessel disease, acute myocardial infarction (AMI), and cardiogenic shock were randomized to PCI of the culprit lesion only (with potentially staged PCI for non-culprit lesions) or to immediate multi-vessel PCI (including non-culprit artery lesions) in the period from April 2013 to April 2017. Non-culprit artery lesions may be regarded, with some caveats, as having pathologic characteristics largely resembling lesions found in patients with stable angina.…”

Section: Editorialmentioning

confidence: 99%

“…The currently on-going ISCHEMIA trial addresses this question in thousands of patients including many with multi-vessel disease but results will not be available until some years later. However, indirect tangential evidence has emerged from the recent CULPRIT-SHOCK trial [9].In CULPRIT-SHOCK [9], 706 patients with multi-vessel disease, acute myocardial infarction (AMI), and cardiogenic shock were randomized to PCI of the culprit lesion only (with potentially staged PCI for non-culprit lesions) or to immediate multi-vessel PCI (including non-culprit artery lesions) in the period from April 2013 to April 2017. Non-culprit artery lesions may be regarded, with some caveats, as having pathologic characteristics largely resembling lesions found in patients with stable angina.…”

mentioning

confidence: 99%

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Can PCI Ever Replace Optimal Medical Therapy in Treating“ Stable” Epicardial Coronary Stenosis?

Wong¹

2017

Cardiovasc Pharm Open Access

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EditorialIn 2007, the COURAGE trial was published showing that in the 2287 randomized patients with stable coronary disease PCI was no better than medical therapy in altering outcome over a median followup period of 4.6 years [1]. The same mortality rate observed among the 2 randomized groups held true at late median follow-up of 6.2 years amongst the 1211 patients with available survival data [2]. One major criticism of COURAGE is that PCI (including the nature of the deployed stents and adjunctive pharmacological therapy) has evolved so rapidly in the last 10 years that the COURAGE findings are no longer applicable today. Modern drug eluting stents plus appropriately potent antiplatelet regimes have ensured almost 100% procedural successes with <1% stent thrombosis and low restenosis rates. Prior editorials in the Journal have discussed some of these aspects [3][4][5][6]. It is tempting for one to think that PCI with stenting will fix any stable epicardial coronary stenosis relieving myocardial ischemia with measurable clinical benefit. However, 2 recent trials have reported somewhat unexpected results.In the ORBITA trial [7], a double-blinded, multicentre randomised trial of real PCI versus "sham PCI" for angina relief at 5 UK study sites, symptomatic patients with severe (≥ 70% diameter narrowing) singlevessel stenosis were enrolled. They first received 6 weeks of medical therapy optimisation followed by cardiopulmonary exercise testing, symptom questionnaires, and dobutamine stress echocardiography. Then, they were randomised 1:1 to undergo PCI or a placebo procedure. In both groups fractional flow reserve (FFR) and instantaneous flow reserve (iFR) were measured. These FFR and iFR measurements required introducing special coronary wires across the coronary lesion so all patients actually needed the cath lab procedures. Patients were sufficiently sedated together with "auditory isolation" that they were unaware as to whether they received real or sham PCI. Six weeks after the procedure the aforementioned non-invasive assessments were repeated. The primary endpoint was difference in exercise time increment between groups.Of 230 patients enrolled, 200 were finally randomised in the period from January 2014 to August 2017 after completing the medication optimisation phase. The coronary lesions had mean area stenosis of 84·4%, FFR of 0·69 (FFR <0.75-0.8 generally considered significant indicating myocardial ischemia in the subtended territory), and iFR of 0·76 (iFR <~0.9 generally considered significant). All PCI procedures were successful but the primary endpoint, exercise time increment between groups (PCI minus placebo), was only non-significantly higher by 16·6 seconds (P=0.20).Intervention trials with "clinical procedures" are almost always confounded because of the absence of patient blinding unless sham procedures are performed in the control group with all their implications. In the hypertension field, there had been high hopes for renal denervation until it was refuted by the sham-procedure controlled S...

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Section: Editorialmentioning

confidence: 78%

Section: Editorialmentioning

confidence: 98%

Section: Editorialmentioning

confidence: 99%

Section: Editorialmentioning

confidence: 99%

mentioning

confidence: 99%

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Can PCI Ever Replace Optimal Medical Therapy in Treating“ Stable” Epicardial Coronary Stenosis?

Wong¹

2017

Cardiovasc Pharm Open Access

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Cardiogenic Shock After Acute Myocardial Infarction

Samsky

Morrow

Proudfoot

et al. 2021

JAMA

Self Cite

176

101

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ardiogenic shock (CS) is defined by systemic hypoperfusion and tissue hypoxia due to cardiac dysfunction. The most common etiology of CS is acute myocardial ischemia due to occlusion of an epicardial coronary artery, resulting in regional cardiac myocyte necrosis (acute myocardial infarction [AMI]) and loss of ventricular function. 1 CS is the leading cause of in-hospital death in patients with AMI. Between 40 000 and 50 000 patients in the US have CS associated with AMI each year, which correlates to an incidence of approximately 5% to 10% of all patients with AMI. [2][3][4][5] Thirty-day mortality is nearly 40% and approaches approximately 50% at 1 year (Box). [5][6][7][8] Severe left ventricular (LV) dysfunction is the most common presentation of CS in the setting of AMI, most frequently occurring after anterior MI. Of the 686 patients included in the Percutaneous Coronary Intervention Strategies with Acute Myocardial Infarction and Cardiogenic Shock (CULPRIT-SHOCK) trial, 288 (42.0%) had a left anterior descending MI and 53 (7.7%) had a left main coronary artery MI. 7 Few treatment approaches reduce short-or long-term morbidity and mortality in patients with CS. This review describes the pathophysiology, diagnosis, and management of CS in the setting of AMI. MethodsA literature search was performed that applied the Cochrane Highly Sensitive Search Strategy for randomized clinical trials (RCTs), a string for meta-analyses and systematic reviews, and established Medical Subject Headings for "cardiogenic shock" and "treatment" to the PubMed and Cochrane databases for articles published from January 1, 1995, through August 5, 2021. The literature search identified 1552 articles. The authors prioritized RCTs, meta-analyses, and larger observational studies. A total of 46 papers were included, including 12 randomized trials, 2 metaanalyses, 1 systematic review, and 31 observational studies.

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Effect of Intra-arrest Transport, Extracorporeal Cardiopulmonary Resuscitation, and Immediate Invasive Assessment and Treatment on Functional Neurologic Outcome in Refractory Out-of-Hospital Cardiac Arrest

Bělohlávek

Šmalcová

Rob

et al. 2022

JAMA

334

227

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Key PointsQuestionIn patients with witnessed refractory out-of-hospital cardiac arrest, does early intra-arrest transport, extracorporeal cardiopulmonary resuscitation, and invasive assessment and treatment improve outcomes compared with standard resuscitation?FindingsIn this randomized clinical trial that included 256 patients, survival with neurologically favorable outcome (Cerebral Performance Category 1-2) at 180 days occurred in 31.5% in the invasive strategy group and 22.0% in the standard resuscitation group, a difference that was not statistically significant.MeaningAmong patients with refractory out-of-hospital cardiac arrest, the bundle of early intra-arrest transport, extracorporeal cardiopulmonary resuscitation, and invasive assessment and treatment did not significantly improve survival with neurologically favorable outcome at 180 days compared with standard resuscitation, although the trial was possibly underpowered to detect a clinically relevant difference.

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PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock

Cited by 854 publications

References 26 publications

Can PCI Ever Replace Optimal Medical Therapy in Treating“ Stable” Epicardial Coronary Stenosis?

Can PCI Ever Replace Optimal Medical Therapy in Treating“ Stable” Epicardial Coronary Stenosis?

Cardiogenic Shock After Acute Myocardial Infarction

Effect of Intra-arrest Transport, Extracorporeal Cardiopulmonary Resuscitation, and Immediate Invasive Assessment and Treatment on Functional Neurologic Outcome in Refractory Out-of-Hospital Cardiac Arrest

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