RHYTHM PUZZLE
Now you see it, now you don't
T.A. Simmers, A.A.M. Wilde
Figure 1.
An otherwise healthy 66-year-old male was referred with complaints of central chest pain. He was not on any medication, and there were no risk factors for coronary artery disease. Pain invariably occurred at rest T.A. Simmers A.A.M. Wilde Amsterdam Medical Centre, Department of Cardiology, Amsterdam
Correspondence to: T.A. Simmers Amsterdam Medical Centre, Department of Cardiology, P0 Box 22660, 1100 DD Amsterdam E-mail: [email protected]
c
Netherlands Heart Journal, Volume 13, Number 5, May 2005
and subsided spontaneously within approximately 15 minutes. Physical examination, laboratory testing, resting ECG and stress test were all within normal limits; myocardial perfusion scintigraphy revealed no ischaemia. During hospitalisation the patient experienced a recurrence, atwhich time an ECG (figure 1) was taken. En route to emergency coronary angiography the ECG normalised and the symptoms resolved. Angiography showed no significant coronary stenosis. What is the most likely diagnosis? What diagnostic and/or therapeutic measures should be taken? Answer You will find the answer on page 202. 195
RHYTHM PUZZLE
Answer to the rhythm puzzle on page 195 The most striking feature of this ECG is the STsegment elevation and T-wave inversion in leads V1 to V5, aVL and aVR with reciprocal depression in the inferior leads. Findings suggest transmural ischaemia caused by a proximal left anterior descending artery (LAD) lesion. The patient's history of pain at rest, the ECG during pain and (lack of) findings at coronary angiography together lead to a diagnosis of variant or Prinzmetal angina, in this case electrocardiographically due to proximal LAD spasm. The mainstay oftherapy is vasodilative medication (i.e. nitrates and calcium channel blockers) and statins and ACE inhibitors for
202
their effects on the endothelium. Second-line therapy using coronary artery stenting or even brachytherapy has been demonstrated to be ofvalue in drug-refractory cases. Acetylcholine provocation confirmed the diagnosis in this patient, when proximal LAD spasm was observed even on the aforementioned drugs. A stent was placed at the site of spasm during the same procedure. The patient remains free of symptoms after six months of follow-up. m Acknowledgement We are indebted to our colleagues at the Diakonessenhuis Utrecht for this ECG and patient referral.
Netheriands Heart Journal, Volume 13, Number 5, May 2005 cIC
Now you see it, now you don't
T.A. Simmers, A.A.M. Wilde
Figure 1.
An otherwise healthy 66-year-old male was referred with complaints of central chest pain. He was not on any medication, and there were no risk factors for coronary artery disease. Pain invariably occurred at rest T.A. Simmers A.A.M. Wilde Amsterdam Medical Centre, Department of Cardiology, Amsterdam
Correspondence to: T.A. Simmers Amsterdam Medical Centre, Department of Cardiology, P0 Box 22660, 1100 DD Amsterdam E-mail: [email protected]
c
Netherlands Heart Journal, Volume 13, Number 5, May 2005
and subsided spontaneously within approximately 15 minutes. Physical examination, laboratory testing, resting ECG and stress test were all within normal limits; myocardial perfusion scintigraphy revealed no ischaemia. During hospitalisation the patient experienced a recurrence, atwhich time an ECG (figure 1) was taken. En route to emergency coronary angiography the ECG normalised and the symptoms resolved. Angiography showed no significant coronary stenosis. What is the most likely diagnosis? What diagnostic and/or therapeutic measures should be taken? Answer You will find the answer on page 202. 195
RHYTHM PUZZLE
Answer to the rhythm puzzle on page 195 The most striking feature of this ECG is the STsegment elevation and T-wave inversion in leads V1 to V5, aVL and aVR with reciprocal depression in the inferior leads. Findings suggest transmural ischaemia caused by a proximal left anterior descending artery (LAD) lesion. The patient's history of pain at rest, the ECG during pain and (lack of) findings at coronary angiography together lead to a diagnosis of variant or Prinzmetal angina, in this case electrocardiographically due to proximal LAD spasm. The mainstay oftherapy is vasodilative medication (i.e. nitrates and calcium channel blockers) and statins and ACE inhibitors for
202
their effects on the endothelium. Second-line therapy using coronary artery stenting or even brachytherapy has been demonstrated to be ofvalue in drug-refractory cases. Acetylcholine provocation confirmed the diagnosis in this patient, when proximal LAD spasm was observed even on the aforementioned drugs. A stent was placed at the site of spasm during the same procedure. The patient remains free of symptoms after six months of follow-up. m Acknowledgement We are indebted to our colleagues at the Diakonessenhuis Utrecht for this ECG and patient referral.
Netheriands Heart Journal, Volume 13, Number 5, May 2005 cIC
