Endothelial dysfunction: the reversible coronary disease

Abstract

Case report. A 59-year-old male experienced sudden dyspnoea and severe chest pain without radiation. He was nauseous and vomited. On his way to the bathroom he collapsed and lost consciousness. By the time the ambulance arrived, ventricular fibrillation was diagnosed. Sinus rhythm was obtained by means of DC cardioversion. Upon arrival at the hospital he was conscious and without severe symptoms. Physical examination revealed a blood pressure of 120/80 mm Hg, a regular pulse of 100 beats per minute, normal heart sounds and normal peripheral pulsations. The ECG showed a regular sinus rhythm with a frequency of 100 beats per minute, normal conduction and slight diffuse ST-depression ( Figure 1). His laboratory tests revealed a creatininekinase of 6374 IU/L with a CKMB fraction of 555 IU/L. Six years earlier he had suffered from two episodes of chest pain for which he had consulted a cardiologist. The exercise test demonstrated slight ST-depression, but no significant stenosis had been seen at coronary angiography. With regard to risk factors for atherosclerosis he was only known to have hypercholesterolemia. He was a non-smoker and his family history was negative.Shortly after admission, coronary angiography (CAG) was performed, showing a similar picture as 6 years earlier with a dominant right coronary artery, a relative narrow left main coronary artery and diffuse non-severe atherosclerosis in the left descending artery and in the left circumflexus artery (Figure 2). The fractional flow reserve of the left main coronary artery was normal (0.92).During a subsequently performed exercise test, the patient experienced severe chest pain during peak exercise, showing 4 mm ST-depression on his ECG ( Figure 3). Myocardial perfusion SPECT scan (MPS) was performed. Again, during exercise the patient felt recognisable chest pain, and shortly after exercise he collapsed suffering from hypotension and severe bradycardia. The Technetium-99m-sestamibi ( 99m Tc) stress-MPS revealed a large perfusion defect stretching from the anterolateral and anteroseptal wall to the apex and inferoposterolateral wall with a LVEF of 37% due to post-ischaemic stunning. The rest-MPS, performed with 201-Thallium-chloride ( 201 Tl), showed complete normalisation of the perfusion defect ( Figure 4).With this picture in mind a new CAG was performed. This provided no new information. An acetylcholine provocation test was performed with selective infusion of acetylcholine in incremental doses into the left main coronary artery. The second injection of acetylcholine with a dose of 10 -5 mmol/L resulted in a severe vasoconstriction of the whole left coronary artery system ( Figure 5). This resulted immediately in ventricular fibrillation. Fortunately, the severe vasospasm responded quickly to intracoronary injections of nitroglycerin. The patient recovered instantly. We interpreted this severe coronary spasm as the cause for his previous episodes of chest pain and VF. Endothelial dysfunction was diagnosed as the underlying cause.Endothelial dysfunction. ...

Let’s functionalize the myocardial flow reserve

“…11 Importantly, functional alterations may be amenable to therapeutic interventions with normalization of the flow reserve. 12,13 Extravascular resistive forces can also oppose hyperemic flow responses when intra-myocardial pressures are high as for example in patients with systolic blood pressure or with elevated left ventricular filling pressures. 14 Functional characterization of impaired flow responses can identify possible mechanisms and guide patient management.…”