When a patient arrives to your ED fresh from karate class still in her uniform, you get a feeling about where the case is heading. This patient was 49, and reported that she always had some aches after karate. This evening, though, her pain was very different — and much more concerning. The pain had started about an hour into her class and worsened over the next 30 minutes. It was a severe achy pain over her left chest that radiated to her neck and was associated with pronounced diaphoresis. This prompted an expedited cardiac workup.
The ECG showed a sinus tachycardia with ST-elevation in V2-V3, I, aVR, aVL, with depression in II, III, aVF, and V5-V6. The ST-elevation in V2-V3 with inferior reciprocal depression (II, III, aVF) was concerning for myocardial injury in the anteroseptal region caused by left anterior descending artery (LAD) occlusion. EPs should have a high suspicion for very proximal LAD, left main, or Circumflex occlusion when seen in conjunction with ST-elevation in I, aVL, and aVR.
She was taken immediately for coronary angiography, and was found to have an extensive thrombosis originating in the left main and extending into the proximal LAD and Circumflex arteries. The clot was removed by aspiration thrombectomy, and further angiography and intravascular ultrasound revealed dissection of the coronary arteries originating in the left main and propagating down the LAD. A small perforation of the LAD was seen just proximal to the first diagonal takeoff.
Spontaneous coronary artery dissection (SCAD) is an uncommon event, and occurs when the layers of the artery separate, creating a false lumen. Hemorrhage into the false lumen propagates the dissection distally. The true lumen of the vessel can become blocked by thrombus or the dissection flap. Obstruction of the lumen reduces perfusion and causes myocardial ischemia and necrosis. Patients present with symptoms of ischemic cardiac chest pain and with associated ECG and enzyme changes typical of NSTEMI or STEMI. ACS is often the initial concern, but the diagnosis of SCAD is made during coronary angiography.
The dissected medial flap shows up as a thin radiolucent line. Overlying thrombus is seen as haziness in the true lumen. SCAD is often treated with percutaneous intervention. Using IVUS, the dissection flap can be identified, and a guide wire can be placed carefully in the true lumen. Stenting open the flap seals the dissection, preventing further propagation, restoring flow in the true lumen, and relieving ischemia. Coronary artery bypass surgery is often difficult. Grafting to the true lumen is difficult with long dissections, and the vascular tissue is often too fragile to support suturing.
Atherosclerotic plaque rupture can cause complex intramural hematoma formation in the vascular wall dissecting the layers, but the dissection rarely propagates much further than the extent of the atheroma. More commonly, though, dissection associated with atherosclerotic plaque rupture can occur during balloon angioplasty or PCI. As the vessel is dilated, the fibrous cap and intimal layer can be torn, leading to dissection. Dissection in these scenarios is not usually labeled SCAD.
SCAD, in contrast, is not associated with coronary artery disease. Women make up the majority of cases, and they tend to be younger. A significant percentage occurs in the peripartum period, and the LAD is the most affected coronary artery. SCAD has also been associated with Marfan syndrome, fibromuscular dysplasia, and peripheral eosinophilia disease.
Unfortunately for our patient, she had profound cardiogenic shock and was emergently placed on VA ECMO (which I will cover in the future) despite thrombectomy and stenting of the dissection flap. She had little recovery of her cardiac function over the next two weeks, and was transitioned to a left ventricular assist device (LVAD) as destination therapy.
LVADs provide mechanical pump support for patients with severe heart failure as permanent treatment or a bridge to therapy. The most common device used today is the HeartMate II (Thoratec). It uses a continuous flow axial pump that is implanted in the abdominal wall. The inflow cannula (relative to the pump) draws blood from the apex of the left ventricle, and the blood is pumped through the outflow cannula into the proximal ascending aorta.
(New Engl J Med 2007;357:885.)
The pump is powered and controlled by an external controller and batteries that are connected to the implanted pump by a driveline. Important parameters reported by the LVAD are pump speed (RPM), power, pulsatility index, and flow estimate.
Patients with LVADs can present to the emergency department for any condition. The most important rule for evaluating a patient with an LVAD is to assess the patient as you would normally, completely independent of the device. Specific assessment of the LVAD itself is shown in Table 1, and common LVAD complications are listed in Table 2.
The patient did well, and she was discharged home after several more weeks in the hospital. She maintains close follow-up in the LVAD clinic and close contact with her LVAD coordinator. She is being evaluated for an underlying connective disorder.