The patient is a 56-year-old man with hypertension, diabetes, and obesity who was admitted 6 months ago to an outside hospital with a late presentation of an anterior MI. He presented approximately 3 days post MI and underwent cardiac catheterization at 1 week, which showed a total occlusion in the mid-left anterior descending artery (LAD), severe stenoses of the first and second diagonals, and no significant disease in either the right coronary artery (RCA) or left circumflex artery (LCx). The patient was then referred to your hospital for revascularization. The patient, however, failed to show for his appointment and finally presented 8 months later with CP and SOB. Prior to revascularization you order a positron emission tomography (PET) rubidium (Rb)/fluorodeoxyglucose (FDG) using Rubidium82 /F18A (flourine-18–labeled deoxyglucose) to determine the degree of inducible ischemia and viability. The images obtained are in Figure below.
Rubidium/FDG PET scan with the stress images displayed on top, the rest images next, and the delayed metabolic FDG images displayed on the bottom.
The images from the PET scan demonstrate:
Hibernating myocardium in the LAD territory. There is a matched defect in the LAD territory seen on the resting and post-stress images involving the apex and four periapical segments as well as the mid-anterior and anteroapical segments. This is consistent with a large LAD territory infarct without any inducible ischemia. The metabolic FDG images show a perfusion/metabolism mismatch with FDG uptake seen in the previously mentioned LAD segments, suggesting a large region of hibernation in the LAD territory without any significant scar. (Note that there is significant gastrointestinal [GI] uptake near the inferior wall.) The degree of hibernation involved 40% of the myocardium (6% for each involved segment except for the apex, which represents 4% of the myocardium). A study by Hachamovitch et al. 1 in 2003 showed that revascularization was superior to medical therapy if the amount of myocardium at risk (ischemic and hibernating) exceeded 20%. Since the above patient demonstrated a large area of hibernating myocardium in the LAD territory, the patient would benefit from revascularization of the LAD territory as well as the diagonals. This patient underwent surgical revascularization of all three vessels.
The patient is a 75-year-old man with hypertension, diabetes, hypercholesterolemia, and coronary artery disease (CAD) who is 10 years s/p CABG: left internal mammary artery to LAD, saphenous vein graft (SVG) to RCA, and SVG to first obtuse marginal. He is asymptomatic on a good medical regimen, although he is relatively sedentary. TTE demonstrated normal LV systolic function with left ventricular ejection fraction (LVEF) 60%, moderately severe left ventricular hypertrophy (LVH), and no significant valvular disease. The patient is now sent for cardiac evaluation prior to surgery on his dilated abdominal aorta (7.5 cm in diameter). An adenosine nuclear stress test is ordered for preoperative risk assessment. During the adenosine stress he remained asymptomatic although he developed 2-mm ST depressions in I, L, and V2–V6 . There were no significant changes in blood pressure. Figure below shows the scan.
The scan demonstrates:
Multivessel ischemia. The resting scan showed GI activity, but overall normal tracer uptake. There was increased septal uptake caused by the moderately severe LVH. Post stress there is severely reduced tracer uptake involving the mid- and apical anterior, entire anteroseptal, and inferolateral walls and inferior wall and apex. There was also cavity dilation post stress. This is known as transient ischemic dilation (TID). The gated images that accompanied this study demonstrated hypokinesis of the above segments. Note that the post-stress gated images are acquired post stress, but at rest. That is to say that there is a delay between stress and imaging, which may allow for some recovery of function. This scan is of high risk in that there is ischemia in all three vascular territories with TID and extensive wall motion abnormalities. Although the patient was asymptomatic under his baseline conditions, it was appropriate to order the adenosine nuclear stress test since the patient is diabetic with prior revascularization and with a questionable functional status who was going to undergo a high-risk surgical procedure (aortic aneurysm repair).
The patient is a 62-year-old man with CAD risk factors including diabetes (16 years), hypertension, family history of CAD, and obesity. The patient had a silent inferior MI 2 years earlier detected by ECG. The patient is now sent for preoperative evaluation for bilateral knee surgery. The patient has no CP with exertion; however, his exercise capacity is limited by knee pain. He does occasionally have mild post-prandial dyspnea. His medications include insulin, a statin, an angiotensin-converting enzyme inhibitor, a βblocker, and an aspirin. A pharmacologic dual-isotope (Thal/Tc) scan was performed and is shown in Figure below.
A pharmacologic (adenosine) dual-isotope (Thal/Tc) scan with the stress images displayed on top with the resting images below.
The gated images showed an LVEF of 42% with a wall motion abnormality in the inferolateral wall. There were no ECG changes or symptoms during the adenosine infusion. The rest and post-stress images demonstrate
Scar and ischemia in the LCx/RCA territory. The full interpretation of the study was that there was marked GI activity in the rest images, but there was also a severe resting perfusion defect involving the basal and midinferolateral segments. Although GI activity can make the basal and midinferior segments difficult to interpret at rest, the post-stress images clearly show that the defect now involves the entire inferolateral and inferior walls, showing infarct with peri-infarct ischemia in the LCx/RCA territory. Cardiac catheterization demonstrated a total obstruction of the proximal LCx (a dominant LCx) with collaterals from the RCA and LAD. There were no obstructions in the RCA and LAD. Important points from this case include that diabetics are at high risk for CAD and clinical parameters do not predict ischemia (from the detection of ischemia in asymptomatic diabetes (DIAD) trial). Myocardial perfusion imaging can be performed safely post MI to assess infarct size and the amount of myocardium at risk. It is also a good test to assess the adequacy of collateral blood flow.
The patient is a 60-year-old man with hypertension, diabetes (newly diagnosed), and CAD (s/p percutaneous coronary intervention with drugeluting stent in his mid-LAD 5 years ago, and bare metal stent to distal RCA, and a posteroventricular branch 7 years ago). The patient is now sent for symptom evaluation. The patient notes the onset of CPs with exertion while playing squash approximately 2 months ago. The pain occurs only with activity and resolves within a few minutes with rest. He denies other associated symptoms or discomfort at rest. A treadmill nuclear stress test was performed. The patient exercised using a standard Bruce protocol having completed eight metabolic equivalents and reached 98% maximum predicted heart rate (MPHR). There was a normal ST-segment response to stress, and there was no CP with exercise. He did, however, develop new ST depressions in recovery and new atrial fibrillation in recovery, requiring treatment with β-blockers. The scan images are shown in Figure below.
An exercise technetium-99m nuclear stress test with the stress images with the gated images (currently still) on top, the post-stress images next, and the resting images on the bottom.
The appropriate interpretation of this scan is:
LAD and LCx versus left main ischemia. The resting images demonstrate normal perfusion. Post stress, however, there are significant perfusion defects in the anterior, anterolateral, and inferolateral walls. There is also cavity dilatation, which is consistent with either left main disease or multivessel ischemia. The gated images showed new wall motion abnormalities in the LAD and LCx territories. The presence of stressinduced perfusion defects in multiple vascular territories as well as TID and new wall motion abnormalities on the gated images are all findings associated with high-risk scans. The cardiac catheterization in this patient demonstrated 70% stenosis in the proximal LAD, while the stent in the mid- LAD was patent. There was a large obtuse marginal with a 90% proximal stenosis. There was mild disease in the proximal RCA, and the stents in posterior descending artery and posteroventricular branch were patent.
A 19-year-old young woman is referred to your office for evaluation of congestive heart failure (CHF) and MR. She has a history of complete heart block and has previously undergone pacemaker implantation. On physical examination, her heart rate is 85 bpm, respiratory rate of 16, and blood pressure 108/65 mmHg. Her jugular venous pulse is visible 6 cm above the sternal angle at 45 degrees. The point of maximum impulse is sustained but normal in location. She has a grade II/VI holosystolic murmur at the apex that radiates to the axilla. There is trivial bilateral pedal edema. A posterior– anterior and lateral chest X-ray demonstrates mild cardiomegaly. A TTE reveals moderately reduced LV systolic function with an EF of 35%. There is 2+ to 3+ posteriorly directed MR. A cardiac CT with contrast is obtained to evaluate the coronary arteries (Fig. below A and B).
A. Double-oblique image of the aortic root at the level of the right and left sinuses of Valsalva. Ao, aorta; LA, left atrium; RCA, right coronary artery; RVOT, right ventricular outflow tract. B. Oblique axial image at the level of the left coronary artery origin. LCA, left coronary artery.
Which of the following is true regarding this patient’s condition?
Patients with this condition who survive past childhood often present with varying degrees of heart failure, myocardial ischemia, and MR, depending on the development of collateral circulation. This CT demonstrates an anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Also known as Bland-White-Garland syndrome, ALCAPA is a rare but serious congenital anomaly. It is caused by either (a) abnormal septation of the conotruncus into the aorta and PA or (b) persistence of the pulmonary buds together with involution of the aortic buds that eventually form the coronary arteries. Occurrence is similar between men and women and is not considered an inheritable congenital cardiac defect. Because of the low pulmonary vascular resistance, left coronary artery flow reverses and enters the pulmonic trunk (coronary steal phenomena). As a result, the LV myocardium remains underperfused, leading to infarction of the anterolateral LV wall. This often causes anterolateral papillary muscle dysfunction and variable degrees of mitral insufficiency. Consequently, the combination of LV dysfunction and significant MV insufficiency leads to CHF symptoms (e.g., tachypnea, poor feeding, irritability, and diaphoresis) in the young infant. Collateral circulation between the right and left coronary systems eventually develops. Approximately 85% of patients present with clinical symptoms of CHF within the first 1 to 2 months of life. Left untreated, the mortality rate in the first year of life is 90% secondary to myocardial ischemia or infarction and MV insufficiency leading to CHF. In unusual cases, the clinical presentation with symptoms of myocardial ischemia may be delayed into early childhood. Rarely, a patient may stabilize following infarction and may present with MV regurgitation, periodic dyspnea, angina pectoris, syncope, or sudden death later in childhood or even adulthood, as in this patient. Treatment consists of surgical ligation of the anomalous coronary artery origin and bypass grafting to the left coronary artery. Reimplantation onto the native aortic root is typically not possible because of the friable quality of the anomalous left coronary artery ostium.
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