Elevation of Left-Sided Diaphragm Leading to Myocardial Infarction by Compression of the Left Circumflex Artery

Author Affiliations: From the Department of Cardiology, Heart Centre, University of Dresden, Germany. The authors report no conflicts of interest regarding the content herein. Manuscript submitted December 7, 2007, provisional acceptance given March 24, 2008, and accepted March 25, 2008. Address for correspondence: Dr. med. S. P. Schoen, Department of Cardiology, Heart Centre, University of Dresden, Fetscherstr. 76 - 01307 Dresden, Germany. E-mail: cardiology@email.de

_______________________________________________ ABSTRACT: A previously healthy 46-year-old male presented to our emergency department with severe thoracic pain, dyspnea and vomiting, which had suddenly started 2 hours before. He had no history of unusual features and no cardiovascular risk factors. The 12-lead electrocardiogram indicated a posterolateral myocardial infarction. Immediate coronary catheterization revealed occlusion of the proximal left circumflex artery (LCX). Recanalization and coronary stent implantation were successful. No other coronary lesions were detectable that could have indicated coronary artery disease. During catheterization, superposed intestinal loops in the left thorax were striking. The chest X-ray revealed crass cranial displacement of the left-sided diaphragm with intestinal loops beneath, leading to compression of the ipsilateral lung and to a mediastinal shift to the right. Thoracic computed tomography showed compression by the elevated diaphragm of the posterior atrioventricular groove and the left circumflex (LCX) artery embedded in this. Clinical workup revealed no muscular disorder or central dysfunction responsible for diaphragm elevation; no reason for a phrenic nerve lesion was found. The patient subsequently developed ventilatory failure, necessitating intermittent noninvasive bilevel positive airway pressure. After 5 days of intermittent ventilation, the elevation of the diaphragm reduced noticeably and respiratory assistance could be stopped. The cause of this reversible unilateral diaphragm elevation remained unknown.

_______________________________________________

J INVASIVE CARDIOL 2008;20:E250–E252 Case Report. A previously healthy 46-year-old male presented to our emergency department with severe thoracic pain, dyspnea and vomiting, which had suddenly started 2 hours previously. He did not complain of fever, cough or abdominal pain. The patient’s history had no unusual features or cardiovascular risk factors. Physical examination showed a man in good condition with shortness of breath during talking and at rest. His temperature was 36.8°C, pulse 102 beats per minute, respiratory rate 30–40 breaths per minute and blood pressure 110/60 mmHg. His cardiovascular system was normal. Auscultation of the lungs revealed decreased breath sounds at the left base and bronchial breath sounds on the left side. No crackles, rhonchi, or wheezing were found. The 12-lead electrocardiogram (ECG) showed ST-segment elevation in leads II, III, aVF and V4–V6. As we suspected myocardial infarction, the patient was immediately transferred to the catheterization laboratory. Coronary catheterization demonstrated occlusion of the proximal left circumflex artery (LCX). After passage of a guidewire, balloon angioplasty and implantation of a coronary stent, TIMI 3 blood flow was achieved (Figure 1). No other coronary lesions were detectable that might have indicated the presence of coronary artery disease. During catheterization, distorted coronary arteries and superimposed intestinal loops in the left thorax were striking. A chest X-ray revealed crass cranial displacement of the left-sided diaphragm with distended intestinal loops beneath, compressing the ipsilateral lung and shifting the mediastinum to the right (Figure 2). Thoracic computed tomography (CT) was performed to differentiate an elevated diaphragm from thoracic herniation and to identify possible causes for a phrenic nerve lesion. It was striking that the left-sided diaphragm was severely elevated, leading to compression of the posterior atrioventricular groove and of the LCX embedded in this (Figure 3). Clinical workup revealed no muscular disorder or central dysfunction responsible for diaphragm paralysis, and no cause for phrenic nerve lesion was visualized on CT. The patient subsequently developed ventilatory failure, necessitating treatment with intermittent noninvasive bilevel positive airway pressure. Thoracoscopic diaphragm plication was considered; however, after 5 days of intermittent ventilation, the elevation of the diaphragm greatly decreased and respiratory assistance could be stopped. The cause of reversible unilateral diaphragm elevation remains unknown. The patient made a full recovery and was discharged 8 days after presentation. Discussion. Unilateral diaphragmatic paralysis is often asymptomatic and is recognized as unilateral elevation of the diaphragm on chest X-ray. However, it is uncommon for cardiac compression due to an elevated diaphragm to lead to coronary occlusion. To the best of our knowledge, this is the first case of coronary occlusion caused by severe unilateral elevation of the left-sided diaphragm to be reported in the literature. There are some previous reports that cardiac compression from gastrointestinal causes can cause hemodynamic compromise. Kalra et al reported a case of a strangulated gastric volvulus, causing cardiac compression and resulting in electromechanical dissociation.1 The patient was successfully resuscitated, followed by surgical repair with a good outcome. Two other case reports described cardiac compression following cardiac surgery due to an unrecognized hiatus hernia.2,3 The patient reported by Devbhandari3 developed hemodynamic instability and ST-segment elevation on ECG due to cardiac compression from a hiatus hernia. Insertion of a nasogastric tube and decompression of the stomach resulted in rapid and dramatic improvement in the patient’s condition and ST-segment changes resolved completely. In the present case, ST-segment elevations also indicated myocardial infarction. Coronary catheterization revealed occlusion of the proximal LCX. The underlying pathomechanism may have been diaphragm elevation, leading to compression of the posterior atrioventricular groove and the LCX embedded in this. A causal link between the unilateral elevation of the diaphragm and the coronary occlusion is highly probable in the absence of cardiovascular risk factors and arteriosclerotic lesions in a young and healthy male. Furthermore, thoracic CT showed direct compression of the posterior atrioventricular groove by the elevated diaphragm. Paralysis of a hemidiaphragm results from interruption of transmission of the phrenic nerve and can have infectious, iatrogenic or malignant causes, or be linked to bony deformities or subdiaphragmatic pathology. Nevertheless, the most common cause is paralysis of unknown etiology.4 Thoracic CT was performed to differentiate the elevated diaphragm from thoracic herniation and to identify possible causes leading to a phrenic nerve lesion. Clinical workup revealed no muscular disorder or central dysfunction responsible for diaphragm elevation, and no cause for a phrenic nerve lesion was visualized on CT. The patient subsequently developed ventilatory failure and treatment with intermittent noninvasive bilevel positive airway pressure became necessary. It is known that diseases that affect diaphragmatic function may impair the ability of the respiratory muscles to generate pressure.5 Unilateral diaphragmatic paralysis is usually well tolerated. However, under conditions of increased loads, severe unilateral diaphragm elevation can cause dyspnea and hypoxemia and require treatment. Symptoms and outcomes are improved by treatment with noninvasive ventilation.5 Furthermore, thoracoscopic diaphragm plication was considered.6 However, after 5 days of intermittent ventilation, the elevation of the diaphragm lessened noticeably and respiratory assistance could be stopped. As in most cases, the cause of reversible unilateral diaphragm elevation remains unknown.4 The patient made a full recovery and was discharged 8 days after presentation.

1. Kalra PR, Frymann R, Allen DR. Strangulated gastric volvulus: An unusual cause of cardiac compression resulting in electromechanical dissociation. Heart 2000;83:550.
2. Hasegawa Y, Saito T, Horimi H, et al. Hiatal hernia incarceration during cardiopulmonary bypass in patient with acute aortic dissection. Nippon Kyobu Geka Gakkai Zasshi 1995;43:1680–1683.
3. Devbhandari MP, Khan MA, Hooper TL. Cardiac compression following cardiac surgery due to unrecognised hiatus hernia. Eur J Cardiothorac Surg 2007;32:813–815.
4. Fraser RS, Muller NL, Colman N, Pare PD. The diaphragm. In: Diagnosis of Diseases of the Chest, Vol. IV. Philadelphia: WB Saunders Company, 1999, pp. 2987–3010.
5. Celli BR. Respiratory management of diaphragm paralysis. Semin Respir Crit Care Med 2002;23:275–281.
6. Freeman RK, Wozniak TC, Fitzgerald EB. Functional and physiologic results of video-assisted thoracoscopic diaphragm plication in adult patients with unilateral diaphragm paralysis. Ann Thorac Surg 2006;81:1853–1857.