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Active inflammatory bowel disease and coronary artery dissection
  1. M Srinivas1,
  2. P Basumani1,
  3. R Muthusamy2,
  4. N Wheeldon3
  1. 1Department of Gastroenterology, Rotherham District General Hospital, Rotherham, UK
  2. 2Department of Cardiology, Rotherham District General Hospital, Rotherham, UK
  3. 3South Yorkshire Cardiothoracic Centre, Sheffield, UK
  1. Correspondence to:
 Dr M Srinivas
 Department of Gastroenterology, Rotherham District General Hospital, Moorgate Road, Rotherham S60 2UD, UK;


The case of a young woman with flare-up of Crohn’s disease, who had an acute myocardial infarction due to the spontaneous dissection of the left anterior descending coronary artery, is reported. The literature on this rare condition is reviewed and a mechanism postulated for spontaneous coronary artery dissection in inflammatory bowel disease.

  • AST, aspartate aminotransferase
  • LAD, left anterior descending
  • coronary artery dissection
  • myocardial infarction
  • Crohn’s disease

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Spontaneous coronary artery dissection is an uncommon condition, presenting as chest pain with features of acute myocardial infarction, acute coronary syndrome, or cardiogenic shock. We report the case of a young woman with flare-up of Crohn’s disease, who subsequently developed features of acute myocardial infarction due to spontaneous dissection of the left anterior descending (LAD) coronary artery. To our knowledge, there are no case reports of spontaneous coronary artery dissection in active inflammatory bowel disease in the medical literature.


A 35 year old Caucasian woman was admitted with a four day history of bloody diarrhoea, vomiting, and abdominal pain. There was no fever, chest pain, palpitations, or shortness of breath. There were no epidemiological risk factors for infective diarrhoea. Crohn’s disease was diagnosed in 1995, involving small bowel and transverse and descending colon, based on radiological findings (barium enema and ultrasonography). There had been only one admission, in 2000, since diagnosis. The only risk factor for coronary artery disease was smoking 10 cigarettes daily for 11 years. At the time of this admission, she was on maintenance treatment with balsalazide and a reducing course of prednisolone (10 mg once a day), started for a recent flare. Physical examination was unremarkable except for mild epigastric tenderness with no signs of intestinal obstruction, abdominal mass, or organomegaly. Clinically, a differential diagnosis of flare-up of Crohn’s disease or infective diarrhoea was considered.

Laboratory investigations (reference range), on admission, revealed a white cell count of 18.3 (4−11) ×109/l with predominant neutrophilia, platelet count 485 (150−400) ×109/l, plasma viscosity 1.89 (1.46−1.81), C-reactive protein 274 (1−10) mg/l, albumin 25 (34−46) g/l, aspartate aminotransferase (AST) 159 (13−37) IU/l, creatinine 242 (55−96) μmol/l, and urea 9.1 (2.8−7.4) mmol/l. Chest and abdominal radiographs were normal. Stool samples for microscopy, culture, and Clostridium difficile cytotoxin were subsequently reported negative. Creatine kinase and electrocardiography were not done on admission as cardiac pathology was not suspected.

On the first day she was treated with intravenous fluids, antiemetics, and metronidazole. However, on the second day, the patient developed palpitations and central chest pain without haemodynamic compromise. An electrocardiogram revealed sinus rhythm and, surprisingly, ST segment elevation in V1–V3 leads and Q waves in V1–V3 and aVL, suggestive of a recent anteroseptal myocardial infarction (fig 1). Creatine kinase was raised at 1320 (29−198 IU/l) and troponin T 5.58 (<0.1 ng/ml). The patient was not considered for thrombolysis because of bloody diarrhoea with active colitis, but she was transferred to the South Yorkshire Cardiothoracic Centre at Sheffield for primary angioplasty.

Figure 1

 Electrocardiogram with features of a recent anteroseptal myocardial infarct.

Coronary angiography revealed spontaneous dissection of the proximal LAD artery extending over a large diagonal vessel (fig 2). The LAD was stented and the diagonal artery was angioplastied. The rest of the coronaries were normal.

Figure 2

 Coronary angiogram showing LAD dissection extending over a marginal artery (white block arrowhead).

She made an uneventful recovery and the flare-up of Crohn’s disease settled with an increased dose of prednisolone (30 mg once a day). On day 7, the C-reactive protein had dropped to 13 from 274 mg/l with complete normalisation of full blood count, renal and liver function.

An echocardiogram showed a left to right shunt through a small atrial septal defect with no chamber enlargement and normal left ventricular function. An optimal exercise test at six weeks was negative for exercise induced ischaemia and arrhythmia. At a recent review, nine months later, the patient remains asymptomatic with good control of the inflammatory bowel disease and no recurrence of chest pain.


Spontaneous coronary artery dissection was first described by Pretty in 1931.1 The majority of the patients are women in their 30s and at least one third are pregnant or postpartum.2,3 Causes of spontaneous coronary artery dissection include systemic hypertension, coronary spasm, aortic root dissection, fibromuscular hyperplasia, Marfan’s syndrome and connective tissue diseases, but in several cases no cause has been identified (idiopathic). Coronary artery dissection has also been reported during coronary angiography, percutaneous coronary interventions, bypass surgery, and blunt trauma to the chest.4 There is one case report of coronary artery dissection after prolonged retching.5 Left coronary artery involvement is commoner in women and right coronary artery in men. The LAD artery is affected in 80% followed by the right coronary artery and the left circumflex artery.6,7 Our patient is the first reported case of coronary artery dissection in inflammatory bowel disease to the best of our knowledge. She did not have any of the previously mentioned causes of coronary artery dissection. It is quite possible that the dissection was idiopathic or induced by an early atheroma because of smoking. This was not demonstrated on angiography and an intravascular ultrasound was not indicated in this case. Features supportive of a flare-up of Crohn’s disease in this patient were polymorphonuclear leucocytosis, thrombocytosis, and hypoalbuminaemia. The steep rise in C-reactive protein in our patient was probably reflective of the inflammation in the gut and the site of coronary dissection. This is supported by a drop in C-reactive protein to 50 mg/l within 72 hours of LAD stenting, without an increase in the dose of prednisolone. Subsequently, a further drop in C-reactive protein to almost normal levels and control of diarrhoea was achieved by increasing prednisolone to 30 mg daily. The LAD may have been dissecting asymptomatically on admission or earlier, compromising coronary blood flow, as evidenced by a disproportionately high AST on the day of admission. The patient developed symptoms 24 hours later, when the dissection had become severe enough to cause flow restriction in the LAD artery territory.

Crohn’s disease is a well recognised prothrombotic state causing venous and arterial thromboses.8 Histological evidence in Crohn’s disease and coronary artery dissection support inflammatory cell infiltration in the affected cell walls. It remains debatable if it is the cause or effect in the latter.8,9 We postulate that active Crohn’s disease may predispose patients to spontaneous coronary artery dissection by the release of proinflammatory cytokines causing intramedial haemorrhage and thrombosis due to rupture of vasa vasorum.10 The luminal pressure exerted by the shearing effect of this intramedial damage, in a normal coronary artery, can lead to dissection due to the absence of the stenting effect of an atheroma. Continued smoking probably contributed to the severity of the flare-up of Crohn’s disease, vascular inflammation, and thrombogenicity in this case.

Learning points

  • Spontaneous coronary artery dissection is uncommon, but can be fatal.

  • It should be suspected in young female patients with chest pain and electrocardiographic changes consistent with myocardial infarction in the absence of significant risk factors for coronary artery disease.

  • Crohn’s disease, due to its proinflammatory predisposition, may precipitate coronary artery dissection by cytokine release and this aspect needs further research.


This case highlights the silent progress of dissection to critical stenosis. In many cases of sudden death due to spontaneous coronary dissection, the diagnosis is made only at necropsy. While idiopathic coronary artery dissection is probable, active systemic inflammation is a possible aetiology for spontaneous coronary artery dissection in our patient with otherwise normal coronary arteries. Spontaneous coronary artery dissection may be yet another extraintestinal manifestation of Crohn’s disease.


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