Tag Archives: cardiology


Testing of Low-Risk Chest Pain Patients

A summary of the literature on low risk chest pain, including history, physical exam, ECG, biomarkers, and investigations such as exercise tolerance testing, myocardial perfusion imaging, and other investigations, is provided in the American Heart Association’s recently published scientific statement.

The document contains a number of useful statistics on the limitations of clinical assessment in ruling out coronary artery disease, such as these:

…the Multicenter Chest Pain Study found that 22% of patients presenting with symptoms described as sharp or stabbing pain (13% with pleuritic pain and 7% with pain reproduced on palpation) were eventually diagnosed with ACS.”

Testing of Low-Risk Patients Presenting to the Emergency Department With Chest Pain
A Scientific Statement From the American Heart Association

Circulation. 2010;122:1756-1776 – Full Text

Hypothermia and hypokalaemia

We all like to treat selected post cardiac arrest patients with hypothermia now, but isn’t hypothermia associated with a drop in potassium, which of course can precipitate pesky ventricular dysrhythmias in patients who would really rather not arrest again. Maybe the hypothermia itself is protective against the dysrhythmias?

A study from the Mayo Clinic updates our knowledge of this area:

METHODS: We retrospectively analyzed potassium variability with Therapeutic Hypothermia (TH) and performed correlative analysis of QT intervals and the incidence of ventricular arrhythmia.

RESULTS: We enrolled 94 sequential patients with OHCA, and serum potassium was followed intensively. The average initial potassium value was 3.9±0.7 mmol/l and decreased to a nadir of 3.2±0.7 mmol/l at 10 h after initiation of cooling (p<0.001). Eleven patients developed sustained polymorphic ventricular tachycardia (PVT) with eight of these occurring during the cooling phase. The corrected QT interval prolonged in relation to the development of hypothermia (p<0.001). Hypokalemia was significantly associated with the development of PVT (p=0.002), with this arrhythmia being most likely to develop in patients with serum potassium values of less than 2.5 mmol/l (p=0.002). Rebound hyperkalemia did not reach concerning levels (maximum 4.26±0.8 mmol/l at 40 h) and was not associated with the occurrence of ventricular arrhythmia. Furthermore, repletion of serum potassium did not correlate with the development of ventricular arrhythmia.

CONCLUSIONS: Therapeutic hypothermia is associated with a significant decline in serum potassium during cooling. Hypothermic core temperatures do not appear to protect against ventricular arrhythmia in the context of severe hypokalemia and cautious supplementation to maintain potassium at 3.0 mmol/l appears to be both safe and effective.

Hypokalemia during the cooling phase of therapeutic hypothermia and its impact on arrhythmogenesis
Resuscitation. 2010 Dec;81(12):1632-6

Magnesium in asthma limits tachycardia

Dr WFS Sellers and colleagues describe several cases that demonstrate convincingly a protective effect of intravenous magnesium sulphate against the tachycardia produced by intravenous salbutamol in patients with asthma. This effect was observed both when magnesium was given before and when given after the salbutamol. It was seen in critically ill asthmatic patients and in a volunteer with well-controlled asthma.

Intravenous magnesium sulphate increases atrial contraction time and refractory times. It is used to treat atrial tachyarrhythmias and has a negative chronotropic and dromotropic effect.

Intravenous magnesium sulphate prevents intravenous salbutamol tachycardia in asthma
Br J Anaesth. 2010 Dec;105(6):869-70

CPAP in LVF again

Another stab at assessing noninvasive ventilation in cardiogenic pulmonary oedema has been made by Italian researchers who compared CPAP with noninvasive pressure support ventilation (nPSV – similar to BiPAP) in a randomised trial of  80 patients. The primary outcome was endotracheal intubation rates. There was no significant difference between the two modalities. This result is in keeping with the much larger 3CPO trial.

Continuous Positive Airway Pressure vs. Pressure Support Ventilation in Acute Cardiogenic Pulmonary Edema: A Randomized Trial
J Emerg Med. 2010 Nov;39(5):676-84

GPIIb/IIIa inhibitors

A systematic review on use of GPIIb/IIIa inhibitors in NSTEACS has been updated as part of the Annals of Emergency Medicine‘s Evidence Based Emergency Medicine series. The bottom line:

In patients with non-ST-segment elevation acute coronary syndromes who do not undergo early percutaneous coronary intervention, administration of platelet glycoprotein IIb/IIIa (GPIIb/IIIa) inhibitors, given in addition to aspirin and unfractionated heparin, does not reduce 30-day or 6-month mortality. For the composite endpoint of myocardial infarction or death, there was modest benefit at 30 days and 6 months; however, there was an increased risk of major hemorrhage among those receiving GPIIb/IIIa inhibitors.

Update: Use of Platelet Glycoprotein IIb/IIIa Inhibitors in Patients With Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction
Annals of Emergency Medicine Volume 56, Issue 5 , Pages e1-e2, November 2010

Compare this with the recommendations of the European Resuscitation Council who provide the following summary regarding this class of drug:

Gp IIB/IIIA receptor inhibition is the common final link of platelet aggregation. Eptifibatide and tirofiban lead to reversible inhibition, while abciximab leads to irreversible inhibition of the Gp IIB/IIIA receptor. Older studies from the pre-stent era mostly support the use of this class of drugs. Newer studies mostly document neutral or worsened outcomes. Finally in most supporting, as well as neutral or opposing studies, bleeding occurred in more patients treated with Gp IIB/IIIA receptor blockers. There are insufficient data to support routine pre-treatment with Gp IIB/IIIA inhibitors in patients with STEMI or non-STEMI-ACS. For high-risk patients with non-STEMI-ACS, in-hospital upstream treatment with eptifibatide or tirofiban may be acceptable whereas abciximab may be given only in the context of PCI. Newer alternatives for antiplatelet treatment should be considered because of the increased bleeding risk with Gp IIB/IIIA inhibitors when used with heparins.

European Resuscitation Council Guidelines for Resuscitation 2010 Section 5. Initial management of acute coronary syndromes
Resuscitation 81 (2010) 1353–1363 – full text downloadable

McConnell’s sign revisited

In acute pulmonary embolism, a well-recognised pattern of right ventricular wall motion reported by McConnell is characterised by normal RV apex (RVa) contractility with akinesia of the RV free wall. A study using an echo techique called longitudinal velocity vector imaging (VVI) was conducted to describe RVa mechanics in relation to the rest of the RV in patients with a proven acute PE (aPE) and to compare these results to healthy volunteers and to patients with known chronic pulmonary hypertension (cPH). There were no significant differences in segmental strain patterns between the aPE and cPH groups. The authors suggest that McConnell’s sign is probably a visual illusion; preserved RVa contractility might be due to tethering of the RVa to a hyperdynamic left ventricle in the presence of an acutely dilated RV and this is the most likely explanation of the regional pattern of RV dysfunction seen in aPE patients.

Video describing McConnell’s sign from YouTube:

Right Ventricular Apical Contractility in Acute Pulmonary Embolism: The McConnell Sign Revisited
Echocardiography. 2010 Jul;27(6):614-20

Fancy new ACS tests

It’s hard to keep track of all new proposed biomarkers that may be useful in the work up of acute coronary syndrome (ACS) patients. We’re all used to troponin now – so we really want to know how novel tests measure up against the existing standard, in particular for the timeframe in which troponin is less helpful, namely the first six hours.
A systematic review examine the evidence for the following biomarkers in the early assessment (ie, within 6 h of symptom onset) of suspected ACS:

  • CK-MB: CK-MB and 2 h ΔCK-MB have potential in diagnosing AMI in the first hours after symptom onset. Whether CK-MB has value in the early diagnostic assessment of ACS in addition to clinical symptoms, ECG or other markers has rarely been studied.
  • myoglobin: myoglobin might be of value in early ruling out of AMI and ACS in suspected patients because of the relatively high NPV; its PPV, however, is low. However, it is not yet known whether myoglobin has diagnostic value in addition to symptoms, signs and other diagnostic tests (eg, ECG), because of the lack of multivariable analysis
  • heart-type fatty acid binding protein (H-FABP): H-FABP seems to have some potential as an early diagnostic marker of AMI or ACS, but its value in addition to clinical features and other markers has not been studied
  • ischemia modified albumin (IMA): IMA could be a potential marker for early ruling out of ACS in chest pain patients because of its relatively high NPV, especially combined with cTn and ECG. However, its PPV is low. Importantly; IMA seems to add relevant diagnostic information to more readily available diagnostic parameters. However, problems with the stability of IMA and its lack of cardiospecificity have been reported
  • pregnancy-associated plasma protein A: contradictory results indicate that the diagnostic value of PAPP-A in patients suspected of having ACS has not been evaluated properly
  • glycogen phosphorylase isoenzyme BB: GPBB might be a marker for myocardial ischaemia and myocardial necrosis, although the available research is limited and does not assess the added value of the marker.
  • myeloid-related protein 8/14: more research is needed to evaluate the (added) diagnostic value of MRP 8/14 in patients suspected of having ACS.

The authors also point out the introduction of high-sensitivity troponin assays may further improve diagnosis of ACS. They refer to a study in patients with suspected AMI presenting at the emergency department, which showed that a sensitive cTnI assay had a higher NPV than a standard cTnT assay and comparable PPV for detecting AMI within 6 h of symptom onset. The PPV was 79.3% and 80.7%, respectively; the NPVs were 95.3% and 88%. The Full Text of this high-sensitivity troponin paper is here

The review makes the following conclusions:

  • current guidelines advocate the use of cardiac troponin or CK-MB when cTn is not available, and myoglobin in the first 6 h in addition to cTn
  • IMA and H-FABP seem to be promising diagnostic biomarkers in the early diagnostic assessment of patients suspected of having ACS
  • There is an urgent need for adequately designed studies of (novel) ACS markers and their combinations against contemporary troponin assays

Novel biochemical markers in suspected acute coronary syndrome: systematic review and critical appraisal
Heart. 2010 Jul;96(13):1001-1

Inferior MI – check V1 too

Lead V1 directly faces the right ventricle and during an inferior AMI may exhibit ST elevation with concomitant right ventricular infarction. Lead V1 also faces the endocardial surface of the posterolateral left ventricle, and ST depression may reflect concomitant posterolateral infarction (as the “mirror image” of ST elevation involving posterolateral epicardial leads). In this situation, V3 also shows ST depression. In lead V1, however, ST elevation from right ventricular AMI may potentially cancel out the ST depression from posterolateral AMI to give an isoelectric ST level. Diagnosis of right ventricular infarction during an inferior AMI may therefore be aided by evaluating both V1 and V3 ST levels. Both right ventricular infarction and postero-lateral infarction worsen the prognosis of an inferior AMI.

In 7967 patients with acute inferior myocardial infarction in the Hirulog and Early Reperfusion or Occlusion-2 (HERO-2) trial, V1 ST levels were analyzed with adjustment for lead V3 ST level for predicting 30-day mortality.

V1 ST elevation at baseline, analyzed as a continuous variable, was associated with higher mortality. Unadjusted, each 0.5-mm-step increase in ST level above the isoelectric level was associated with ~25% increase in 30-day mortality; this was true whether V3 ST depression was present or not. The odds ratio for mortality was 1.21 (95% confidence interval, 1.07 to 1.37) after adjustment for inferolateral ST elevation and clinical factors and 1.24 (95% confidence interval, 1.09 to 1.40) if also adjusted for V3 ST level. In contrast, lead V1 ST depression was not associated with mortality after adjustment for V3 ST level. V1 ST elevation ≥1 mm, analyzed dichotomously in all patients, was associated with higher mortality. The odds ratio was 1.28 (95% confidence interval, 1.01 to 1.61) unadjusted, 1.51 (95% confidence interval, 1.19 to 1.92) adjusted for V3 ST level, and 1.35 (95% confidence interval, 1.04 to 1.76) adjusted for ECG and clinical factors. Persistence of V1 ST elevation ≥1 mm 60 minutes after fibrinolysis was associated with higher mortality (10.8% versus 5.5%, P<0.001).

The authors conclude that V1 ST elevation identifies patients with acute inferior myocardial infarction who are at higher risk, although because no myocardial imaging was performed, could only speculate that the mechanistic link between V1 elevation and increased mortality is due to the occurrence of right ventricular infarction.

This is important to know about in terms of prognostication, but is it useful in the diagnosis of right ventricular AMI? The authors acknowledge that the ECG diagnosis of right ventricular infarction is classically made by recording lead V4R. In an autopsy study of 43 patients, ST elevation in lead V4R had higher sensitivity and specificity than ST elevation in lead V1 in diagnosing right ventricular infarction. Similarly, ST elevation in leads V7 through V9 adds significantly to precordial ST depression in aiding the diagnosis of posterolateral AMI. The authors contend that recording leads V4R and V7 through V9 is an additional step in the performance of a standard 12-lead ECG and, although recommended, may not be routinely performed.

I will continue to do a V4R in all inferior AMIs, and a V7-8 at least in patients with ST depression in V1-3.

Prognostic Value of Lead V1 ST Elevation During Acute Inferior Myocardial Infarction
Circulation. 2010 Aug 3;122(5):463-9

Unilateral pulmonary oedema worse

A few years ago in the Emergency Department I managed a sick hypotensive, hypoxic 20-something year old with a unilateral lung white-out and air bronchograms as pneumonia/septic shock. He died subsequently of refractory pulmonary oedema on the ICU, where the diagnosis of acute pulmonary oedema due to severe aortic stenosis was delayed. Post mortem findings showed pulmonary oedema but no pneumonia. A kind radiologist told me the chest x-ray would certainly have fitted with pneumonia. After this case I learned to echo sick hypotensive patients in the ED.

Circulation reports 869 cardiogenic pulmonary oedema patients, of which 2.1% had unilateral pulmonary oedema (UPE). In patients with UPE, blood pressure was significantly lower (P<=0.01), whereas noninvasive or invasive ventilation and catecholamines were used more frequently (P=0.0004 and P<0.0001, respectively). The prevalence of severe mitral regurgitation in patients with bilateral pulmonary edema and UPE was 6% and 100%, respectively (P<0.0001). In patients with UPE, use of antibiotic therapy and delay in treatment were significantly higher (P<0.0001 and P=0.003, respectively). In-hospital mortality was 9%: 39% for UPE versus 8% for bilateral pulmonary edema (odds ratio, 6.9; 95% confidence interval, 2.6 to 18; P<0.001). In multivariate analysis, unilateral location of pulmonary edema was independently related to death.

Prevalence, Characteristics, and Outcomes of Patients Presenting With Cardiogenic Unilateral Pulmonary Edema
Circulation. 2010 Sep 14;122(11):1109-15

Balloon pump before PCI? Nah.

High risk patients benefit from pre-operative intra-aortic balloon counterpulsation (IABP) prior to coronary artery bypass surgery. Would the same apply to patients undergoing percutaneous coronary intervention (PCI)?
A multicentre randomised controlled trial was conducted on over 300 patients with severe LV dysfunction and extensive coronary disease. The intervention was elective insertion of IABP before PCI. The composite primary end point of death, acute myocardial infarction, cerebrovascular event, or further revascularization at hospital discharge was not reduced in the intervention group.
These results do not support a strategy of routine IABP placement before PCI in all patients with severe left ventricular dysfunction and extensive coronary disease.

Elective Intra-aortic Balloon Counterpulsation During High-Risk Percutaneous Coronary Intervention
JAMA. 2010;304(8):867-874