Spontaneous Circulation focuses on advanced ECG interpretation, cardiac pharmacology, hemodynamic assessment and resuscitation, and managing acute coronary syndrome. It is devoted to translating the best evidence-based treatments from critical care, resuscitation, and trauma for bedside use in the emergency department.
Monday, July 07, 2014
Our patient was having an uneventful and ordinary day. He got his children off to school, and spent the morning at the office completing paperwork. By noon he had eaten lunch, and went to the company workout center. It was Wednesday, so it was arms day. He started as he always did with 20 minutes of cardio on the elliptical machine, then shoulders, biceps, triceps, forearms — big muscle to small muscle. It was at the end of his first rep of triceps that things changed.
He felt some dizziness, and the nausea began within 30 seconds or so. He couldn't hold himself upright, and slouched sideways off the bench onto the ground, losing consciousness. Others had seen him slide to the floor, and tended to him immediately. He did not have a pulse, and chest compressions were started. Another person ran to get an AED, which advised a shock. A jolt of electricity and remarkably he had a pulse and regained consciousness.
He was brought by ambulance to the ED, and said he felt fairly well besides minor chest wall pain from the CPR. The patient didn't have exercise-related chest pain or chest tightness, and denied a sense of racing heart or palpitation prior to the event. He had not had any previous known cardiac history or previous exertional syncope. He had no family history of premature coronary artery disease, cardiomyopathy, or sudden cardiac death.
Vital signs and physical exam were unremarkable. A 12-lead ECG was obtained. (Figure 1.) The ECG shows sinus rhythm with some right axis deviation and nonspecific ST-T changes; otherwise no current of injury, infarction pattern, or ischemic changes were seen. QTc is not prolonged, and no Brugada pattern or evidence of Wolf-Parkinson-White are present.
Figure 1. 12-lead ECG on presentation to the emergency department
An emergent transthoracic echocardiogram was performed, and a parasternal long axis view is shown in Figure 2. Left ventricular hypertrophy was present, systolic function was at the lower limits of normal, and he had a mild asynchronous kinesis of the septum. Most notably, he had an inferolateral wall motion abnormality, with a suggestion of thinned myocardium over the segment.
Figure 2a and 2b
Watch videos of an emergent transthoracic echocardiogram in the parasternal long axis view here and here. Left ventricular hypertrophy was present, systolic function was at the lower limits of normal, and he had a mild asynchronous kinesis of the septum.
Myocardial segments with abnormal enhancement or wall motion disturbances are named and localized according to the 17 segments-model of the American Heart Association. In cross-section, the left ventricle can be divided into apex, mid, and basal sections, and then subdivided circumferentially. (Figure 3.) Individual myocardial segments can be assigned to the three major coronary arteries with the recognition that anatomic variability exists.
Figure 3. Left ventricle segment definitions.
Given the concern for coronary artery disease, coronary angiography was performed and showed no significant coronary artery disease. LVEDP was 20, and no evidence of gradient across aortic valve was seen. The initial working diagnosis was possible catecholaminergic polymorphic ventricular tachycardia (CPVT) because it followed intense exercise. Given the echocardiographic finding, this is likely to be scar-mediated, probably from previous silent myocardial infarction with possible recanalization. This can best be evaluated with a cardiac MRI. (Figure 4.)
Figure 4. Cardiac MRI.
One of the benefits of cardiac MRI is the ability to evaluate the myocardium’s response to Gadolinium contrast. The contrast is taken up in normal and injured myocardium, but it is washed out easily of normal tissue. There is a delay in eliminated the contrast in certain conditions (approximately 10-15 minutes), and is termed delayed enhancement.
The pattern of the delayed enhancement provides insight to the etiology causing the damaged myocardium. Ischemic cardiomyopathy is seen as ventricular dysfunction in a coronary artery distribution. Tissue involvement always progresses from the subendocardium through to full transmural thickness, depending on the extent of injury. Both acute and chronic myocardial infarctions demonstrated delayed enhancement. The contrast in acute infarctions enters the damaged myocardial cells through the leaky myocyte membrane, but in chronic infarctions the late enhancement is a result of retention of contrast in the fibrous interstitium. On the other hand, nonischemic myocardial disease usually does not occur in patterns consistent with a coronary artery distribution and often can be limited to midwall or epicardial regions. (Figure 5.)
Figure 5. Patterns of delayed enhancement on cardiac MRI.
Delayed enhancement can also identify two important features of ischemic myocardium: stunning and hibernation. Myocardial stunning can occur following an acute myocardial infarction despite restoration of coronary artery flow. The myocytes are dysfunctional, but can regain contractile function over time. The myocardial function is likely to improve if the delayed enhancement is less than 50 percent of the transmural thickness. Hibernating myocardium, however, occurs in chronic ischemic heart disease. Myocytes that are chronically deprived of oxygen can enter a low-energy sleep state; this is potentially reversible by revascularization. Hibernating myocardium can be identified on MRI as areas that do not enhance with contrast. The function is likely to improve after revascularization if the nonenhancing thickness is greater than 50 percent of the transmural thickness.
The cardiac MRI delayed images for our patient show an akinetic segment of marked myocardial thinning in the inferolateral wall of the mid left ventricle with near transmural delayed enhancement. (Figure 6.) This is consistent with sequelae of previous myocardial infarction, and indicates nonviable myocardium in this territory. There was no evidence for an acute or recent myocardial infarction.
Figure 6. Delayed image from patient’s cardiac MRI.
The patient later reported treating himself for heartburn several months before his cardiac arrest, which could have been an unrecognized acute coronary event that resulted in scarring. The cardiac arrest appears to be a primary arrhythmic event probably mediated by a myocardial scar. He was treated with aspirin, beta-blockade, ACE inhibitor, and high-intensity statin even in the absence of underlying obvious coronary disease based on the presence of myocardial scar and suspicious previous symptoms. An ICD was placed for secondary prevention of sudden cardiac death.
Wednesday, June 04, 2014
She watched the Camry coming straight at her, obeying the laws that Newton laid out: a body in motion stays in motion until an external force intercedes.
Her husband, daughter, and the TV weatherman had told her not to go out. Ice had descended on the city earlier in the day, making even the walk to the garage precarious. But she needed milk to make a cake for the next day’s party, and the store was only three blocks away. Her plan was simple: store, milk, home. That might have worked if not for the Camry that became a hockey puck on the ice.
The next couple of hours were a blur but proceeded as readers would expect: 911, paramedics, backboard, cervical collar, ambulance, IV, medicine, stabilization bay, ultrasound, x-rays, more medicine, scanner, hospital bed. All she remembered from that first day through her fentanyl fog was someone saying, “Only a fractured hip. With surgery, this should all be a bad memory in a year.”
She had suffered an acetabular fracture and femoral head fracture. (Figures 1 and 2.)
Figure 1. Pelvic AP x-ray.
Figure 2. Still image from CT scan showing details of acetabular fracture and femoral head fracture.
The next morning she developed atrial fibrillation with a rapid ventricular rate. (Figure 3.) Surgery was postponed, and cardiology was consulted. She was asymptomatic and maintained normal blood pressure despite the rhythm change. The ECG showed diffuse ST-segment depression concerning for subendocardial ischemia, which could be attributed to her known coronary artery disease. She had suffered an NSTEMI about four years earlier, and had two stents placed in the proximal- and mid-RCA. She also had diffuse LAD and circumflex disease. The atrial fibrillation and rapid rate were felt to be secondary to adrenergic stimulation. This improved with additional pain control and beta-blockade, and she spontaneously converted to normal sinus rhythm.
Figure 3. ECG on hospital day 2 when the patient developed atrial fibrillation with rapid ventricular rate.
On hospital day 5, her physicians thought she was safe for surgery, and she underwent a successful ORIF of the posterior acetabulum and total hip arthroplasty. But then she developed chest pain, diaphoresis, and nausea on post-op day 1. Her heart rate slowed to 30 bpm, and she was hypotensive: 90 mm Hg systolic. She responded to a 1000 mL bolus of 0.9% saline and atropine. A 12-lead ECG was obtained.
She awoke the day after surgery hopeful, looking forward to beginning recovery. Breakfast done and waiting for physical therapy, it started. She felt hot and sweaty for several minutes before the chest pain began, followed by nausea. She knew something was wrong, and the seriousness was reinforced by the number of people in her room scurrying about. Her rate slowed to 30 bpm. Blood pressure was below 90 mm Hg systolic. The rapid response team gave her a 1000 mL bolus of 0.9% saline and atropine with good response. A 12-lead ECG was obtained. (Figure 4.)
Figure 4. ECG on the morning of hospital day 6 showing inferior STEMI.
The ECG shows Q-waves in the inferior leads with ST-segment elevation. The R:S ratio is >1 in the right precordial leads suggestive of a true posterior injury. Reciprocal changes are noted in leads I and aVL. A first-degree atrioventricular block was also present. These changes were diagnostic of an inferior ST-elevation myocardial infarction. The bradycardia and hypotension that the patient experienced is suggestive of Bezold-Jarisch reflex, a common epiphenomenon with inferior infarctions.
A STEMI is a clear indication for emergent revascularization, but factors here complicated the medical decision-making. She was at a very high risk of bleeding given her recent orthopedic surgery. Dual antiplatelet therapy and anticoagulation would exacerbate the bleeding risk, which would persist not only during the angiography but afterward if any intervention were performed. Nevertheless, she was treated with aspirin, and taken to the cardiac catheterization lab with the intention of defining the coronary anatomy and identifying the culprit lesion.
She was found to have diffuse disease in the LAD and circumflex coronary arteries but without high-grade obstructive disease. Patent left-to-right collaterals were also seen, as was a 100% occlusion of the ostium of the RCA. (Figure 5.)
Using balloon angioplasty, this was reduced to 30%, which reestablished flow. (Figure 6.) Unfortunately, a thrombectomy catheter could not cross the lesion. No stenting was performed. Any stent placed, whether bare metal or drug-eluting, would have required dual antiplatelet therapy that would have placed her at high risk of bleeding. The distal RCA was small in caliber, indicating chronic disease. Placing a stent would also have required additional contrast dye, which would have placed the patient at risk for contrast-induced nephropathy. A temporary pacemaker was placed given her episode of bradycardia.
She remained hemodynamically stable, and developed no decrease of her renal function. Troponin I peaked at 17 ng/mL. No other episodes of chest pain occurred. She recovered completely from her hip surgery over the following weeks. A month after her STEMI, she underwent PCI to the RCA ostia and mid LAD without any bleeding complications. She was discharged from the hospital on the first day of spring with snow still covering the ground.
Monday, May 12, 2014
By Charles Bruen, MD
He had been through this before. The patient, a 57-year-old man, had come through the doors of this emergency department many times. He had a favorite seat in triage. He knew what questions the nurse would ask him once he was in a room, and that the doctor would repeat those same questions. Then tests and labs, then moved upstairs for a couple of days before going home, hopefully feeling better. He knew all of this. Today, though, everything he thought he knew was wrong.
He had once considered himself lucky. He even survived a gunshot to the chest as a young man. But that notion had faded long ago. His health had been getting worse for years. He suffered with diastolic heart failure, COPD, and stage 3 chronic kidney disease brought on by years of poorly treated hypertension and diabetes. He had been told during one of his stays in the hospital that he had depression. He didn't doubt it. He had resigned himself to never getting completely well, but the past couple of days had been even worse.
He had not slept in days, and was extremely fatigued. He was unable to catch his breath, and was in mild distress. Oxygen saturations were 70%, which improved with supplemental oxygen by Oxymizer. He was not having any chest pain, and his blood pressure was in the 100s mm Hg systolic, way below his baseline and surprising given that he had not taken his medications for weeks. Exam was remarkable for generalized edema, diffuse crackles, and JVD elevation. Creatinine was nearly twice his baseline, and BNP was extremely elevated. Serial troponin measurements were normal. An ECG and x-ray were obtained and are shown in Figures 1 and 2.
Figure 1. Electrocardiogram on presentation.
Figure 2. AP Chest radiograph on presentation.
The ECG shows a normal sinus rhythm with short PR interval. A Q-wave is present in lead III, and nonspecific T-wave changes show in the precordial leads. It is unchanged in comparison with previous tracings. The chest x-ray shows pronounced cardiomegaly, vascular congestion, and diffuse interstitial opacities consistent with pulmonary edema.
The diagnosis seemed clear. It was the same diagnosis the patient knew, the same diagnosis he had had every other time he had come to the hospital: exacerbation of his diastolic heart failure, with cardiorenal syndrome. He was treated with nitroglycerin and bumetanide/metolazone to promote diuresis. Which worked. Sort of. Despite a large volume of urine output, his shortness of breath was not improving, and his creatinine continued to worsen. A transthoracic echocardiogram was obtained to assess cardiac function and volume status. Watch this video to see the patient’s echocardiogram showing the parasternal long axis view, and this one to see the patient’s echocardiogram showing the parasternal short axis view.)
Given the patient’s body habitus, the transthoracic echocardiogram was a technically difficult study. Echocardiographic contrast agents in this situation can be useful to help with interpretation. Contrast, usually some form of gas bubble that scatters ultrasound waves, is used for two principle reasons: to detect left to right shunts and to opacify the left ventricle to define the endocardial border, which allows better determination of ventricular dimensions, wall motion, and ejection fraction. Contrast is given intravenously, and it needs to transverse the pulmonary circuit to opacify the left ventricle. Larger bubbles are more stable, but the bubbles need to be less than 10 micrometers to pass through the pulmonary capillaries. The bubbles can be stabilized by surrounding them with a durable structure and using inert gases rather than air. Table 1 lists commonly used echo contrast agents.
The echocardiogram with the help of contrast showed normal left ventricular size and performance (ejection fraction of 65%) without any wall motion abnormality. The right atrium and ventricle were markedly enlarged, however, and there was decreased right ventricular systolic contractility. The right-sided dilation was causing significant tricuspid insufficiency. The estimated pulmonary artery systolic pressure was 27 mm Hg above the right atrial pressure. A notable finding was a D-shaped septum, implying a relative increase in right ventricular end-diastolic pressure. These findings were concerning for increased pulmonary arteriolar vascular resistance versus worsening volume overload. The patient underwent a right heart catheterization to assess this.
Pressure tracing from right heart catheterization.
The right heart catheterization showed that the pulmonary artery pressure was 72/31 (mean 46) mm Hg with an occlusion pressure is 18 mm Hg. This indicates essentially high-normal left-sided pressures and severe pulmonary hypertension. Much to everybody’s surprise, the patient, rather than suffering from left ventricular diastolic failure (heart failure with preserved ejection fraction) that would require elevated left ventricular end diastolic pressures, was actually underfilling his left ventricle. The patient had severe pulmonary hypertension with right-sided heart failure (cor pulmonale). Multiple possible etiologies for the patient’s pulmonary hypertension included COPD, chronic cocaine use causing pulmonary fibrosis/ILD, and chronic hypoxia from untreated obstructive sleep apnea. He had a prescription for CPAP, but had refused to wear it. The right ventricle was hypertrophied and dilated, which gives an indication that this was chronic rather than acute. (Table 2.)
Unfortunately for the patient, his right heart failure continued to decompensate. Despite aggressive attempts at reducing the pulmonary hypertension with inhaled prostacyclins and nitrous oxide, he required escalating vasopressor support. He developed refractory shock and multiorgan failure, and his family elected to pursue comfort care measures.
Monday, April 07, 2014
By Charles Bruen, MD
The patient first felt winded one night after doing the dishes. She was breathing so hard by morning that she was barely able to get out of bed. And a cough had started. “The flu” went through her mind. She stayed home from work to rest, but all day she just couldn’t catch her breath. The cough got worse and was making her chest hurt, and she felt her heart racing. She was exhausted by evening, but knew she wasn’t going to be able to sleep. The temperature was below 0°F outside, but she bundled up and drove herself the three miles to the emergency department. Barely able to speak by the time she stepped up to the triage desk, she was only able to get out “You need to slow my heart down.” The nurse knew that look.
The patient sat down hard in the wheelchair rescuing her from the burden of standing. “Medical Resus” was paged overhead, and the nurse rushed the patient back.
A (airway) was clearly intact as the patient was placed on the cart. Everyone knew that B was going to be problem. The monitoring cables were on before most people noticed, and there was an uncomfortable pause for several seconds while everyone in the Resus Bay waited for the first SpO2. 68%. Heart rate 146 bpm. That’s all it took. An IV was placed, and the patient was intubated in the next few minutes. Attention turned to the cause of respiratory failure. An ECG and chest radiograph was obtained, and are shown in Figures 1 and 2.
Figure 1. Presenting ECG.
Figure 2. Chest radiograph.
The ECG demonstrated atrial fibrillation with rapid ventricular response with ST-segment depression in the lateral leads concerning for myocardial ischemia. Bilateral pulmonary infiltrates show on the chest xray, which also shows a double density along the left heart border representing the bulging of the left atrial appendage. Key items on the differential at this point would include decompensated heart failure, acute coronary syndrome, infectious pneumonia, sepsis, and ARDS. A few minutes with the ultrasound revealed this key image. (Click here to see the video.)
A remarkable hypertrophied and calcified mass is on the ventricular side of the mitral valve, with severely impaired opening of the mitral valve during diastole. The anterior leaflet billows while remaining fixed at the commissure, visually described as a “hockey stick.” The patient’s presentation and this ultrasound are diagnostic of severe mitral stenosis. It was once much more common, but the incidence of mitral stenosis has been gradually declining in the United States. The patient has decades of being asymptomatic after the stenosis is initiated. Patients have several more decades once symptoms do occur before they become debilitating. Ten-year survival once this happens, however, approaches 10 percent. (Table 1.)
Most cases of mitral stenosis by far can be attributed to rheumatic disease. The immune response against Group A streptococcal antigens cross-react with structural glycoproteins of heart valves, especially the mitral valve, with leads to an ongoing auto-inflammatory response and destruction of the native valve. The hallmark of rheumatic mitral stenosis is commissural fusion, scarring and thickening of the valve, and shortening and thickening of the tendinous cords. Radiation therapy has quickly become a significant secondary cause of mitral stenosis.
Distinguishing between rheumatic heart and radiation stenosis can be difficult, even after a careful history. Commissural fusion does not seem to exist in radiation-associated mitral stenosis. Radiation also tends not to damage the papillary muscles and chordae tendineae. Radiation, however, tends to cause significantly more valvular calcification. Dyspnea is the most common feature of clinically significant mitral valve stenosis. Exacerbation of symptoms can be precipitated with increased cardiac demand (exercise, stress, critical illness) and atrial fibrillation with rapid ventricular rate. Restriction of the cardiac output causes fatigue, and cough and hemoptysis can be present. Evidence of elevated right and left heart pressures such as pulmonary and lower extremity edema are also often present. The physical exam, however, is not specific for mitral stenosis, and even the classic lowpitched rumbling middiastolic murmur is lost as the mitral stenosis progresses. (Table 2.)
A stenotic mitral valve significantly changes cardiac hemodynamics once the valve area falls to less than 2 cm2 (normal 46 cm2). High velocities and a large transmitral pressure gradient are needed because the entire cardiac output must pass through the stenosis. These higher gradients are generated by increased left atrial pressure in systole and diastole, and are transmitted upstream to the pulmonary vasculature and right side of the heart, causing pulmonary edema, pulmonary hypertension, and elevated central venous pressures. The left ventricular end diastolic pressure remains low from the reduced preload, and cardiac output is therefore depressed despite these higher pressures. The systemic vasculature compensates with higher resistance. The transmitral pressure gradient is a useful indicator of severity:
● Mild: <5 mm Hg
● Moderate: 5-10 mm Hg
● Severe: >10 mm Hg
Ultrasound is the primary means of evaluating mitral stenosis, and several techniques can determine the valve area and transmitral pressure gradient:
● 2D planimetry. The opening area of the valve can be measured in the parasternal short axis view at the level of the mitral. The gain and view must be carefully optimized to avoid underestimating the valve area.
● Pressure half-time (PHT). The prolonged emptying time between the left atrium and left ventricle can be exploited because the time that pressure takes to half of its initial maximum value has been shown to be empirically related to the valve area (MVA=220/PHT). The continuous wave Doppler velocity is measured at the level of the mitral valve in an apical four-chamber view. The pressure gradient is related to the maximum velocity by a simplification of Bernoulli’s equation (p=4V2). The time it takes for the A pressure half-time of 220 msec corresponds to a valve area of 1 sq cm.
● Continuity equation. Uses mitral and aortic flow in addition to the cross-section area of the left ventricular outflow tract to derive the mitral valve area. The area is measured by planimetry and flow measured by Doppler assessment of velocity time integral (VTI). This method is less commonly used because of the accumulation in measurement errors.
● Proximal isovelocity surface area (PISA) method. Utilizes a fluid dynamic feature where accelerating flow forms hemispheres of isovelocities. This utilizes the flow convergence region proximal to the high velocity trans mitral jet in diastole. It is highly accurate but difficult to perform in transthoracic views and best utilized during transesophageal echocardiography.
The transmitral gradients are highly heart rate-dependent, and patients who develop rapid atrial fibrillation can quickly deteriorate. There is reduced filling time, which demands much higher filling pressures, which in turn causes significant pulmonary edema and occasional hemoptysis from pulmonary venous rupture. Treating mitral stenosis is directed at controlling the heart rate and maintaining sinus rhythm (e.g., digoxin, diltiazem, beta-blockade). Left ventricle contractility is generally preserved in mitral stenosis. β-blockade does result in decreased right ventricular contractility, which in pulmonary hypertension can further compromise the cardiac output and systemic blood pressure.
The loss in right ventricle contractility, however, is more than offset by the beneficial effects of reducing the heart rate. Loop diuretics should be used for diuresis and their venodilation effects (mediated by angiotensin II and prostaglandins) to reduce pulmonary vascular congestion. Left atrial dilation and stasis substantially increases the risk of thromboembolism, especially in atrial fibrillation, and therefore anticoagulation is critical. Surgical intervention is ultimately required, and involves carefully choosing balloon mitral valvuloplasty, mitral valve commissurotomy, or mitral valve replacement.
Monday, March 10, 2014
By Charles Bruen, MD
A 64-year-old woman presented to the emergency department with two days of severe nausea, numerous episodes of vomiting, and progressively worsening right upper quadrant/epigastric abdominal pain. She was continuously spitting clear secretions into an emesis bag on arrival in triage. Her 8/10 dull ”ripping” pain originated in the right upper quadrant and radiated in a band-like pattern to her epigastrium. She was not experiencing any chest pain or shortness of breath. Her medical history included hypertension, type 2 diabetes mellitus, recurrent acute pancreatitis secondary to hyperglycemia, peripheral artery disease, and gout. She smoked a pack of cigarettes daily.
Vital signs were blood pressure 123/79 mm Hg, pulse 86 bpm, respiratory rate 20 bpm, temperature 36.8°C, and SpO2 100%. She appeared quite uncomfortable. Her cardiac and chest exams were unremarkable. Her abdomen was soft but tender to palpation maximally in the epigastric region without rebound. Laboratory studies were ordered. An ECG is shown in Figure 1.
Figure 1. Presenting ECG.
This is a regular sinus tachycardia. The QRS axis is normal, but notable biphasic deep inverted T-waves are seen in the anterior precordial leads. The QTc is also very long at approximately 580 ms. These findings were noted to be different from a previous ECG obtained about three weeks earlier. (Figure 2.) The differential diagnosis of deep inverted T-waves is shown in Table 1.
Figure 2. Previous ECG.
If a patient presents with symptoms compatible with ischemic chest pain, there is a strong likelihood that deep inverted T-waves are an indication of reperfusion of a critically occluded LAD. Named Wellens’ syndrome, the inverted T-waves are seen in the anterior precordial leads, typically V2-V4. The QT interval is often prolonged. If Wellens’ waves are captured on ECG, it is usually after the LAD has reperfused and the chest pain has resolved, which is why the pattern is referred to as reperfusion waves. The initial troponins can be elevated because of a period of ischemia before reperfusion. A critical stenosis or ruptured plaque that remains in the LAD despite the reperfusion, however, that is at high risk of reoccluding. This warrants emergent angiography and PCI.
Her initial troponin I was 0.1 ng/mL. Labs were notable only for a lipase 194 IU/L, glucose 272 mg/dL, and WBC 17 k/mm3. Given the concern for acute coronary syndrome, she was given aspirin 325 mg orally and clopidogrel 600 mg orally, and started on heparin infusion. The patient was taken emergently to the cardiac catheterization lab for angiography with anticipation of PCI.
The patient was found to have a left dominant system and type III LAD. The left circumflex was chronically occluded, and she had pronounced left-to-left collaterals from the LAD. The right coronary artery had two areas of severe stenosis in the mid-portion. The patient had two-vessel coronary artery disease, but the LAD and diagonals had only mild diffuse irregularity, and no culprit lesion was suspected based on the ECG. No PCI was performed.
The naming convention for the LAD can be confusing. A type I LAD stops short of the apex of the ventricle. Type II goes to the apex. Finally, type III wraps around the apex and into the inferior interventricular groove to meet the PDA artery. (Figure 3.)
Figure 3. LAD naming convention.
An echocardiogram showed mild decreased left ventricular systolic function and a septal regional wall motion abnormality. The wall motion abnormality did not correspond to a vascular territory because the apex was preserved. This was felt to represent a stress cardiomyopathy (SCM), also referred to as Takotsubo cardiomyopathy. SCM is associated with severe physical (such as severe illness) or emotional stressors that generate a large catecholamine surge. Typically there is apical ballooning and hypokinesis, but it can also be seen as basal or septal hypokinesis. The effects of this wall motion abnormality can be seen on the ECG as ST-segment elevation (STEMI mimic), deep inverted T-waves, or prolonged QTc. Incidence is higher in women, and prognosis for recovery of systolic function is good.
Because no culprit lesion was identified, the dual antiplatelet therapy was stopped. The use of P2Y12 inhibitors in conjunction with aspirin have proven immensely valuable in treating acute coronary syndrome, largely supplanting the GIIb/IIIa inhibitors. Treating the patient in the ED before angiography (“defining the anatomy,” as cardiologists call it) may not be beneficial, however. A percentage of patients who undergo emergent angiography turn out not to have acute coronary syndrome. Treatment with dual antiplatelet therapy is not indicated, and subjects the patient to the risks of the medication, such as bleeding, without any benefit. Treatment with a P2Y12 inhibitor is a relative contraindication in our patient with acute pancreatitis because of the increased risk of hemorrhagic conversion of the pancreatitis. If a patient truly does have acute coronary syndrome, pretreatment with platelet inhibition with clopidogrel does not provide any anti-ischemic benefit, but does allow the time for the metabolism of the medication to its active metabolite.
The benefits of treating a patient with P2Y12 inhibitors are much smaller for the ACS group if there is a short interval between when a suspected diagnosis of acute coronary syndrome is made in the ED until angiography is performed, but the risks for the non-ACS group remain constant. This tradeoff has been shown not to be beneficial for upstream treatment with prasugrel and ticagrelor, though this is an open question for clopidogrel.
Our patient was placed on maximal medical therapy for atherosclerotic disease, and non-emergent PCI of the RCA was performed once the pancreatitis resolved. She had no complications from the antiplatelet therapy. The patient made a complete recovery from her stress cardiomyopathy with return of normal heart function.