cases, IMA levels are commonly increased [5]. Moreover, IMA is a reliable indicator of oxidative stress, but it is poorly specific because substantial increases are commonly observed after a variety of localized or generalized hypoxic circumstances besides myocardial ischemia and PE, includ- ing physical exercise and systemic sclerosis [3,5]. Therefore, the limited positive predictive value of this marker, when evaluated alone, might contribute to further increase ED crowding, with adverse impacts on expenditures and ability to deliver quality and timely care. The correct recognition of the cause of the underlying chest pain and dyspnea has the potential to make the clinical decision making more timely and globally efficient, but the diagnostic accuracy of each biomarker taken singularly does not support the use as an effective risk stratification tool for patients presenting with chest pain at the ED [6]. In this respect, not only larger studies involving a wider patient selection are needed to further clarify these preliminary results, but the introduction of cost-effective diagnostic algorithms characterized by multiple, specific, highly indicative biomarkers, such as the Natriuretic peptides (which are accurate in identifying low- risk PE patients), Dimerized plasmin fragment D (which can safely rule out ongoing thrombosis), and cardiac troponins (at the time of diagnosis, a few PE patients have negative troponin test) might be advisable [7]. In PE patients with increased levels of these cardiac biomarkers, additional investigations might be warranted to prevent right ventricular dysfunction and additional serious complications [7]. Similarly, future studies on coronary artery disease and IMA should be focused on diseases causing an increase in PE-like symptoms and IMA levels.

Giuseppe Lippi MD Martina Montagnana MD Gian Cesare Guidi MD

Sezione di Chimica e Microscopia Clinica Dipartimento di Scienze Morfologico-Biomediche Universita di Verona 37134 Verona, Italy

E-mail addresses: [email protected] [email protected]

doi:10.1016/j.ajem.2008.01.019

References

1. Turedi S, Gunduz A, Mentese A, Karahan SC, Yilmaz SE, Eroglu O, et al. Value of ischemia-modified albumin in the diagnosis of pulmonary embolism. Am J Emerg Med 2007;25:770-3.
2. Lippi G, Guidi GC. The power of negative thinking. Am J Emerg Med 2008;26:373-4.
3. Lippi G, Montagnana M, Guidi GC. Albumin cobalt binding and ischemia modified albumin generation: an endogenous response to ischemia? Int J Cardiol 2006;108:410-1.
4. Boie ET. Initial evaluation of chest pain. Emerg Med Clin North Am 2005;23:937-57.
5. Lippi G, Montagnana M, Salvagno GL, Guidi GC. Potential value for new diagnostic markers in the early recognition of acute coronary syndromes. CJEM 2006;8:27-31.
6. Jaffe AS. Use of biomarkers in the emergency department and chest pain unit. Cardiol Clin 2005;23:453-65.
7. Kucher N, Goldhaber SZ. Risk stratification of acute pulmonary embolism. Semin Thromb Hemost 2006;32:838-47.

A new cardiopulmonary resuscitation method using only Rhythmic abdominal compression is hard

To the Editor,

We read with great interest the article by Geddes et al. concerning a new CPR method using OAC (only rhythmic abdominal compression). However, we note several issues. First, the authors tried investigating how to maintain coronary perfusion when CPA (cardiopulmonary arrest) with ventricular fibrillation had occurred. But the most important objective of CPR is not to maintain coronary perfusion, but it is to protect the brain from the hypoxia so that patients would gain favorable neurolo- gical outcome [1,2]. Thus, we would like to know data about the brain perfusion in their experiments if available. Second, the first action of CPR is to keep airway open. During the time when emergency medical technicians transport patients with cardiac arrest to hospitals, many patients experience the vomiting of their gastric contents because their stomachs are often full and the mask-bag ventilations can cause spouting of the gastric contents. The vomiting sometimes leads to serious respiratory compromise by obstructing upper airway. Abdominal compression procedures may cause a higher risk for the airway compromise due to retrograde propulsion of the gastric contents into oropharyngeal cavity. Third, they provided data about the incidence of rib fractures as adverse effects of CPR. However, this may not be so much important when patients are going to die or not.

Toshikazu Abe MD Yasuharu Tokuda MD, MPH, FACP Shinichi Ishimatsu MD, PhD

Department of Emergency and Critical Care Medicine St. Luke’s International Hospital, Tokyo 104-8560, Japan Clinical Practice Evaluation and Research Center

St. Luke’s Life Science Institute, Tokyo 104-0044, Japan E-mail address: [email protected]

doi:10.1016/j.ajem.2007.12.011

References

1. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an observational study. Lancet 2007;369:920-6.
2. Ewy GA. Cardiocerebral resuscitation: the new cardiopulmonary resuscitation. Circulation 2005;111:2134-42.

The author’s comments:

To the Editor,

Thank you for your interest in our paper.

Regarding brain versus heart: We chose to evaluate standard chest-compression and OAC-CPR on the basis of coronary perfusion in relation to coronary perfusion with the normally beating heart as the standard because this latter is what the animal needs to stay alive. Also in this way, the animal is its own control. We found that OAC-CPR produced more coronary perfusion than standard chest-compression CPR in the same animal. Also, remember from physiology, the pressure that drives blood through the heart and through the brain is the same, namely aortic minus right-atrial pressure. Moreover if there is inadequate coronary perfusion during CPR, Ventricular defibrillation will result in pulseless electrical activity, a condition that NO existing automatic external defibrillator can detect. Regarding regurgitation; we share your concern. However after performing OAC-CPR on more than 20 pigs, we have never encountered regurgitation. The animals were fed the night before the experiment. In future experiments we will feed the pigs during the morning of each experiment and look for regurgitation. To make the test more severe we will feed the animals in the morning and pump air into the stomach to identify any difference.

Recently the King Corp (Noblesville, IN) has announced an endotracheal tube with a balloon that blocks the esophagus. Both the cuff and the balloon are inflated from the same port. We may have the opportunity to try this device. Two additional items are worthy of the note with OAC- CPR: 1) We have not encountered any damage to abdominal organs and 2) OAC-CPR also produces artificial respiration, The OAC-CPR tidal volume is more than twice the respiratory dead space and one breath is produced with

every abdominal compression.

L. A. Geddes ME, PhD, DSc Fellow American College of Cardiology Fellow Royal Society of Medicine

Pheochromocytomas in aortic dissection patients: have they been missing or missed?

To the Editor,

Arterial hypertension (AHT) is the most important risk factor for aortic dissection (AD). Arterial hypertension has been found in approximately 80% of AD patients [1,2]. Typically, AHT is long-standing and poorly regulated in AD patients. Nowadays, such scenario represents an individual catastrophe and a failure of a medical organization because we have more knowledge about AHT than ever as well as good medicament armamentarium against this “silent killer” and, thus, great expectations. Nevertheless, it is sometimes not easy to control Blood pressure , for example, when variations are pronounced. This is true for pheochromocy- toma (pheo), presumably until operation is done.

Increased heart rate up to tachycardia level has been frequently recorded in pheo. “The number of strokes (ie, heart rate) of stroke volume” into the aortic wall is also important in the ethiopathogenesis of AD. (To produce AD, stroke volume really strokes the aortic wall.) Pheo crises seem to have the additional potential for destructive effect upon the aorta because great variations in BP have been known to exert bad influence on prognosis generally. Besides, BP variations during such a small period as 1 second (1 systole and diastole, approximately), known as Pulse pressure, have been accepted as a risk factor for vascular diseases [3].

There are articles showing the onset of acute AD related to physical effort [4,5]. The direct analogy exists between exercise and pheo as the potential triggers of AD. Nevertheless, analogy is striking between cardiovascular actions of catecholamines secreted by pheo and effects of cocaine or amphetamine. Each of them may induce BP elevation and tachycardia, enough to be referred to as a sympathetic crisis/storm, and in such situations, ?-blockers are contraindicated. Numerous case reports under- line the relationship between cocaine and AD [6-10].

Summa summarum, there has been a rule to search for pheo in poorly controlled AHT, and there is also an analogy between pheo and exercise as well as cocaine/amphetamine, that is, well known causes of AD. Thus, a possibility that pheo may cause AD is quite logical and real. Surprisingly, such reports have been scarce. Namely, search for key words “aortic dissection” and “pheochromocytoma” retrieved only 15 results in PubMed, and together with searches in Scopus, Google Scholar, ScienceDirect, Blackwell Synergy, SpringerLink, Oxford Journals, and Cambridge Journals, we finally found only 8 case reports of simultaneous AD and pheo [11-18].

In addition, among the Cardiovascular effects that pheo can cause, AD has not always been recognized, for example, it was not mentioned in a very good article of Mirza [19].

Indeed, both AD and pheo are rare diseases. However, even allowing possibility of 2 or 3 times more such cases in the literature we were not able to get, the reasons are just presented to believe that some of pheos have been overlooked. Of course, there is a pragmatic aspect of this issue: pheo, if found, may be amenable to surgery, with improved prognosis.

Conclusion

1. There is a rationale for both clinicians and pathologists to screen patients with AD for the presence of pheo.
2. Pheochromocytoma might not be such a rare disease if we look for it on the proper place, for example, in high-risk subsets, like patients with AD.

Koracevic Pante Goran MD, PhD Department of Cardiovascular Diseases Medical Faculty University Clinical Centre

Bul. Dr Z. Djindjica 48 Nis 18000, Serbia and Montenegro

E-mail addresses: [email protected]

[email protected]

doi:10.1016/j.ajem.2008.01.035