Category: Cardiology

Angiography After Cardiac Arrest

This is the worst sort of paper – nuggets of truth mired in systematic flaws.  There’s certainly no ill intent by the authors to mislead, it’s simply the nature of this sort of retrospective review.

The PROCAT consortium has been publishing studies of their post-arrest protocols for several years.  They’re huge proponents of early coronary angiography following resuscitation for out-of-hospital arrest – and this is another in a string of articles demonstrating that patients going to coronary angiography after out-of-hospital arrest have improved outcomes.  Of the 1274 patients in their cohort, 745 received early coronary angiography, 447 identified a culprit lesion, and 347 underwent PCI.  The survival rate was 46% in patients undergoing PCI.

However, this number is conflated by other confounding variables known to be associated with good outcomes following cardiac arrest – coronary lesions are likely to be associated with VT/VF, which were also associated with good outcomes.  Additionally, significantly more survivors received therapeutic hypothermia than non-survivors, illustrating the massive problem with viewing this sort of report with anything other than reasoned curiosity: rampant selection bias.  Patients survived because they were selected for interventions based on individualized prognostic features, treatments were not applied evenly across the population.

There is absolutely a subset of OHCA that benefits from early coronary angiography – but this benefit should not be generalized to the inappropriate allocation of resources associated with taking all OHCA to the cath lab after resuscitation.

“Benefit of an early and systematic imaging procedure after cardiac arrest: Insights

from the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) registry”
www.ncbi.nlm.nih.gov/pubmed/22922264

Send Your PE Patient to MRI!

Well, not exactly…but this is at least a “proof of concept” for cardiovascular magnetic resonance and the diagnosis of pulmonary embolism.

Obviously, helical CT has become the standard diagnostic modality for pulmonary embolism due to its rapid acquisition time and high sensitivity.  Unfortunately, contrast-enhanced scans through the thorax carry with them short- and long-term health risks.  So, what about MRI?

This small case series of twelve PE+ patients and twelve healthy controls undergoing CMR showed fair discriminatory power for pulmonary embolism.  On a per-patient basis, sensitivity was 100% – but to best evaluate a diagnostic test, it’s probably important to consider a higher-resolution measure.  On a per-lobe basis, sensitivity was only 71% – with a kappa of only 0.69 for the reading radiologists.

And, then there’s the minor issue that CMR is a 20-minute scan with 10 minutes of post-processing, so even when this is ready for prime-time, it’s still going to have some practical limitations.

“Pulmonary Perfusion Imaging: New Insights Into Functional Consequences of Pulmonary Embolism Using a Multicomponent Cardiovascular Magnetic Resonance Imaging Protocol” 
www.ncbi.nlm.nih.gov/pubmed/23194944

All Elevated Troponins Are Not MI

Have you ever received sign-out on a patient, heparinized, awaiting cardiology consultation – and later, at your leisure, realized the troponin level just barely tips into positive territory and probably has nothing to do with acute coronary syndrome?

I know you have.

This is the cardiology “expert consensus” on interpretation of troponin elevations – 25 pages of clinical summary and 360 references worth of dissecting what an elevated troponin really means.  There’s an hour-long lecture worth giving based on this publication.

The key portions include:
 – Figure 1, which is a nice conceptual overview in which elevated troponins are separated into their “ACS” and “non-ACS” categories.
 – Section 6, which discusses the possible role (if any) for troponins in non-ischemic conditions.
 – Appendix 4, the clinical conditions in which positive troponins are non-cardiac and confounding in origin.

Positive troponins need to be evaluated properly in their clinical context, and this is a lovely (if very, very long) reference document for describing it.

“ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations”
www.ncbi.nlm.nih.gov/pubmed/23154053

The Hazards of Love

“Sexual activity is mechanically dangerous, potentially infectious and stressful for the cardiovascular system.”

Indeed!

According to this retrospective review of 11 years of electronic health records from University Hospital Bern, Switzerland, they identified 445 patients seeking emergency care secondary to sexual intercourse.  The majority of emergency department visits were secondary to suspected infectious etiologies (62%), but neurologic complaints, trauma, and cardiovascular incidents comprised the remaining portion.  

The trauma portion probably speaks for itself without need for additional detail.  There was one myocardial infarction and one aortic dissection.  Among the “various complaints”, two patients were diagnosed with “eczema”.  However, among the neurologic emergencies, there were 12 cases of subarachnoid hemorrhage and 11 cases of – ah – “transient global amnesia”.

All things being equal, at least, sexual activity was only associated with 0.1% of emergency department visits – hardly the most dangerous of potential choices of recreation.

“Sexual activity-related emergency department admissions: eleven years of experience at a Swiss university hospital” 
http://www.ncbi.nlm.nih.gov/pubmed/23100321

Arrhythmogenic Right Ventricular Dysplasia

In young Emergency Department patients with syncope, most of the time, testing is minimal.  Generally, the only universal testing is a pregnancy test and/or an electrocardiogram.

We’ve gotten pretty good at understanding the “life-threatening” causes of syncope in young adults diagnosed by electrocardiography, including:
 – Wolff-Parkinson-White Syndrome
 – Hypertrophic Obstructive Cardiomyopathy
 – Brugada Syndrome
 – Congenital Long QT

But there’s always more, and Arrhythmogenic Right Ventricular Dysplasia is one of those “more” that seems not to be on everyone’s lists.  ARVD is a genetically-inherited abnormality in cardiac desmosomes that leads to fibrofatty deposition in the right ventricle.  It is currently estimated to result in ~5% of the sudden cardiac deaths in adults under age 65, secondary to sustained monomorphic ventricular tachycardia.  The characteristic EKG finding to look out for is, unfortunately, quite subtle – the “epsilon wave”.  These waves are most prominent in V1-V3, and manifest as sharp upward deflections from baseline at the conclusion of the QRS complex.

Very few Emergency Department presentations mix the high-risk needle-in-the-haystack with the low-risk like young adults with syncope, so it’s important to stay alert for these rare ECG findings.

“Impact of new electrocardiographic criteria in arrhythmogenic cardiomyopathy”
www.ncbi.nlm.nih.gov/pubmed/23015790

Still Overpromising Benefit of PCI After Cardiac Arrest

The folks in France have been promoting PCI universally after cardiac arrest for quite some time.  It’s an appealing concept – when you look at subgroups of out-of-hospital cardiac arrest, there’s a significant portion of folks who clearly have a primary cardiac cause, and clearly will benefit from emergency or early PCI.

However, this study inappropriately tries to make the case for all patients to receive PCI and therapeutic hypothermia after out-of-hospital cardiac arrest.  This is a retrospective, cohort study spanning eight years of resuscitation, coordinated between Paris, France and Seattle, Washington.  They used vital records follow-up to determine patient status for each OHCA patient surviving to hospital discharge, and then looked for associations between survival and whether they received PCI or hypothermia in-house.  The most absurd statement is as follows:

“A beneficial survival association was evident among those with and without ST-elevation MI. This finding is provocative given the current debate about whether patients without evidence of ST elevation following resuscitation can benefit from PCI and should undergo early and routine coronary catheterization.”

Retrospective studies such as this suffer from substantial selection bias, in which the patients who are selected for particular therapies have interactions and confounders that simply cannot be controlled or adjusted.  Patients benefit from PCI when they have a disease process amenable to intervention – and this is clearly not every cardiac arrest patient. The patients in this study who received PCI – and hypothermia – likely had specific features that identified them to treating physicians as candidates to benefit from these therapies.

The reasonable conclusion from the data presented is exactly that – cardiac arrest patients that have specific features that make them candidate for these therapies will benefit.  PCI following cardiac arrest should not be considered to be “routine”.

“Long-Term Prognosis Following Resuscitation From Out of Hospital Cardiac Arrest – Role of Percutaneous Coronary Intervention and Therapeutic Hypothermia” 

When Cardiologists Risk-Stratify Heart Failure

This is the “MARKED” score, a multi-marker prognostic risk score derived from emergency department patients presenting with acute dyspnea.  The authors state they’ve presented a “simple, straightforward” score that “may help the treating physician at the ED to decide on urge of intervention, admission, and timing of re-evaluation.”

Sounds perfect!  A valuable tool to determine which patients are at high-risk for short-term mortality, possibly to predict which patients may have unanticipated poor outcomes if discharged home?

Ah, sadly, no.

When these cardiologists risk-stratify heart failure, they’re using 90-day mortality – an endpoint almost certainly irrelevant to acute evaluation of dyspnea.  The authors recognize the “single-center” aspect of their study as a limitation – but, considering this comes from a dedicated “cardiology ED” in Holland, the external validity is extraordinarily limited.  The authors also do not offer any practical suggestion regarding how this score might be used in practice – or how decision-making using this score effectively changes outcomes compared with usual care.

Finally, this “simple” score features the commonly used laboratory tests such as NT-proBNP, high-sensitivty cardiac troponin T, Cystatin-C, high-sensitivity C-reactive protein, and Galectin-3.  It should be no surprise a few authors receive compensation from Roche Diagnostics and ACS Biomarker B.V.

“Multimarker Strategy for Short-Term Risk Assessment in Patients With Dyspnea in the Emergency Department”
www.ncbi.nlm.nih.gov/pubmed/23021334

The End of IABP?

Adding to the “don’t do anything, just stand there!” file, another relatively frequently used cardiovascular support tool – intra-aortic balloon counterpulsation – might be on the chopping block.

Typically used in cases of severe cardiogenic shock secondary to acute myocardial infarction, IABP is used to reduce strain on the stunned myocardium.  The first IABP-SHOCK pilot of 45 patients showed no mortality difference, but a significant improvement in BNP levels with IABP use.  This is the follow-up study, enrolling 600 patients to IABP or best available medical therapy.

Both groups were similarly ill – the IABP group had 6% more anterior STEMIs – and had nearly identical outcomes.  There were 1.5% more survivors in the IABP group, but the p value was 0.69.  Adverse events were similar – although the control group tended towards increased sepsis, which seems a little odd.  There was an expected random assortment of subgroups favoring one therapy or another, but nothing that would seem to be specifically hypothesis generating.

In the end, the authors rather grimly state that, despite some surrogate markers appearing to be improved in the IABP group, there is no evidence to support routine use of IABP in cardiogenic shock secondary to acute myocardial infarction.

“Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock”
http://www.nejm.org/doi/full/10.1056/NEJMoa1208410

FFR(CT) – So Close, Yet So Far

As David Newman will tell you, the additive prognostic and predictive value for stress tests is fairly weak.  CT coronary angiograms are still a test looking for the correct population.  Conventional coronary angiography is expensive, invasive, and clearly not appropriate for the massive population of low risk patients we evaluate.

So, how about a non-invasive test that combines three-dimensional anatomic coronary reconstruction with predictive flow dynamics to identify lesions resulting in ischemia?  This test is CT coronary angiography combined with computed fractional flow reserve.  And, it would be a beautiful thing if it were ready for primetime – but it’s not.

I’ve reviewed a previous trial of FFR(CT).  This is a larger study, published in JAMA, of 285 patients with suspected CAD who underwent CCTA with FFR(CT), followed by conventional coronary angiography with invasive FFR measurement.  Figure 1 summarizes the results relatively succinctly – but essentially, 56 of the 172 FFR(CT) patients with lesions calculated as ischemic were false positives.  On the flip side, 67 of the 80 FFR(CT) patients with lesions calculated as non-ischemic were false negatives.  The per-vessel performance of FFR(CT) basically added no additional diagnostic AUC to CT alone.

The study is sponsed by HeartFlow, and authored by several physicians disclosing conflicts of interest with diagnostic imaging manufacturers.  Unsurprisingly, the authors try to spin the positive out of it in their conclusions and abstract.

“Diagnostic Accuracy of Fractional Flow Reserve From Anatomic CT Angiography“
http://jama.jamanetwork.com/article.aspx?articleid=1352969