Exercise-induced plaque rupture producing myocardial infarction

A 37-year-old man with unstable angina was subjected to coronary angiography. The right coronary artery showed a minor proximal stenosis, but there were no obstructive lesions in the left coronary artery. He developed a small inferior infarction. He was asymptomatic until re-admission 1 month later, 1 hour after a normal exercise test, with anterior myocardial infarction. Acute coronary angiography showed sub-total occlusion of the left anterior descending artery. The occlusion was partially relieved after intracoronary injection of nitroglycerin. Intracoronary infusion of streptokinase had no further effect. Balloon angioplasty was then successfully performed. It is suggested that stress-induced plaque rupture with intimal hemorrhage and secondary spasm resulted in sub-total occlusion of the left anterior descending artery producing the second myocardial infarction.     

Acute myocardial infarction showing total occlusion of right coronary artery and thrombus formation of left anterior descending artery

A 33-year-old Japanese man had an attack of chest pain associated with ST-segment elevation in the inferolateral leads on his electrocardiogram. Emergency coronary angiography showed total obstruction in the mid right coronary artery (RCA) and a movable thrombus in the proximal left anterior descending artery (LAD). We performed emergency percutaneous transluminal coronary angioplasty (PTCA) for the RCA lesion. The operation was successful and we then conducted intracoronary thrombolysis (ICT) with tisokinase 6,400,000 IU for the LAD thrombus. Its size was reduced by ICT. He had an uneventful hospital course. After 1 month, repeat coronary angiography showed no significant stenosis in the RCA nor thrombus in the LAD. A coronary spasm provocation test was performed using acetylcholine. Coronary spasm in the LAD was induced by an intracoronary injection of 100 microg acetylcholine. In this case, we observed a unique condition suggesting simultaneous double coronary artery occlusion.     

Acute myocardial infarction caused by simultaneous occlusion of the right coronary artery and the left anterior descending coronary artery probably due to coronary spasm: a case report

A 56-year-old man had an attack of chest pain associated with ST-segment elevation in both the inferolateral and anteroseptal leads on electrocardiography. Emergency coronary angiography showed thrombus in the mid right coronary artery and total occlusion in the distal left anterior descending coronary artery. Intravenous heparin infusion and antiplatelet therapy were given without other coronary intervention. After 1 week, repeat coronary angiography showed neither significant stenosis nor thrombus in the coronary arteries. Severe coronary artery spasm in the left coronary artery was induced by the provocation test with intracoronary injection of 50 microg acetylcholine. He had an uneventful hospital course. This unique case demonstrated intracoronary thrombus formation in the right coronary artery and left anterior descending coronary artery simultaneously due to suspected coronary spasm.     

Simultaneous multivessel coronary spasm causing acute myocardial infarction: a case report

Spontaneous simultaneous multivessel coronary artery spasm in patients with acute myocardial infarction (AMI) is uncommon. A 79-year-old Japanese man was transferred to this hospital because of severe prolonged chest pain and faintness. Left coronary angiography revealed total occlusion of the left anterior descending and the left circumflex coronary arteries. Moreover, right coronary angiography revealed 99% stenosis of the right coronary artery. After intracoronary administration of nicorandil, left coronary artery and right coronary artery angiography revealed no organic stenosis or thrombus. This is the first report in which simultaneous 3-vessel spasm was documented by emergency angiography in AMI.     

Acute myocardial infarction due to late stent thrombosis seventeen months after stent implantation: a case report

A 59-year-old man with acute myocardial infarction underwent successful stent implantation for proximal left anterior descending coronary artery occlusion. Antiplatelet therapy with 100 mg aspirin/day and 200 mg cilostazol/day was started after stenting and continued for 4 weeks. There was no cardiac event during the 1 year follow-up period. Follow-up coronary angiography at 12 months after stenting revealed no in-stent restenosis. The patient was admitted 17 months later due to sudden onset of severe chest pain. Electrocardiography revealed ST segment elevation in leads V1-V4. Emergency coronary angiography disclosed obstruction of the proximal left anterior descending coronary artery with thrombus. Intracoronary aspiration thrombectomy was successful. We describe a patient with acute myocardial infarction who had late stent thrombosis 17 months after stent implantation.     

Intracoronary thrombolytic therapy: A Treatment Option for Failed Mechanical Thrombectomy

The benefit of the routine application of aspiration thrombectomy in primary percutaneous coronary intervention (PPCI) is now well established. The optimal management of patients who have “failed” thrombectomy characterized by a large residual thrombus burden after repeated mechanical thrombectomy, however, is not known. We report a case of failed aspiration thrombectomy in a 66‐year‐old woman who was admitted to our institution with chest pain associated with inferior ST segment elevation. Coronary angiography showed a thrombotic occlusion of the right coronary artery. Aspiration thrombectomy did little to reduce thrombus load and so the patient was treated with intracoronary tenecteplase. Repeat coronary angiography 18 hr later revealed marked thrombus resolution with thrombolysis in myocardial infarction (TIMI) grade 3 anterograde flow and patency of the infarct‐related artery was maintained at 2‐month follow up. This case demonstrates the potential for intracoronary thrombolytic therapy as a treatment option for the management of patients following failed thrombectomy in PPCI. © 2011 Wiley Periodicals, Inc.     

Severe diffuse coronary artery spasm in the early phase of cardiogenic shock

Coronary artery vasospasm rarely appears as a diffuse phenomenon that involves all the coronary tree. We present a clinical case of acute myocardial infarction complicated by ventricular fibrillation and cardiogenic shock. Urgent coronary angiography showed occlusion of proximal Circumflex coronary artery and a TIMI I flow in the left anterior descending artery due to severe, diffuse coronary vasospasm. Patient was successfully treated with intra-aortic balloon pump and intracoronary bolus of nitroglycerin with restoration of flow in left coronary branches and complete resolution of shock.     

Successful management of the no-reflow syndome after venous graft stenting

The no-reflow phenomenon is often found in venous grafts and every effort to prevent it is worthwhile. We performed an angioplasty on a venous graft in a patient with a NSTE acute coronary syndrome with previous inferior myocardial infarction (1996) and CABG (3 venous grafts ), respectively. The native coronary vessels had significant lesions: 70% left main stenosis, distal circumflex artery occlusion, LAD occlusion after the first diagonal branch and proximal occlusion of the RCA. All of the venous grafts,with the exception of the circumflex, were patent. The latter showed subocclusion and slow flow. This was the culprit lesion for the unstable syndrome. After stenting it, no residual stenosis appeared, but severe no-reflow ensued. The no-reflow phenomenon disappeared after intracoronary eptifibatide infusion and aspiration of the slugging contrast from the vein. Clinically, the patient had no chest pain and his ECG changes normalized.     

Intracoronary infusion of streptokinase in patients with acute myocardial infarction: Effects of reperfusion on left ventricular performance

Cardiac catheterization and coronary angiography were performed on hospital admission in 32 consecutive patients with acute myocardial infarction. Twenty-six patients had total occlusion of an infarct-related coronary artery and six had severe proximal stenosis with poor distal flow. In 18 of the 26 patients with total occlusion, intracoronary infusion of Streptokinase resulted in reperfusion of the distal coronary artery. Seventeen of these 18 patients had severe coronary arterial stenosis at the site of the previous total occlusion. Hemodynamic indexes of left ventricular performance and ejection fraction determined by gated cardiac blood pool imaging did not change immediately after reperfusion (p [probability]= not significant [NS]). The mean (± standard deviation) left ventricular ejection fraction increased significantly (p = 0.007) from admission (44 ± 15 percent) to hospital discharge (55 ± 7 percent) in patients evidencing reperfusion of the occluded coronary artery. It did not change (p = NS) in this time span in the patients with severe stenosis alone, in those with total occlusion not demonstrating reperfusion after administration of streptokinase or in an additional 10 control patients with acute myocardial infarction not evaluated with coronary angiography. These data suggest that (1) coronary arterial thrombus is frequent in acute myocardial infarction and can be lysed by intracoronary streptokinase; (2) reperfusion with intracoronary streptokinase in acute myocardial infarction results in improved left ventricular performance between admission and hospital discharge.     

Late recanalization at the site of failed percutaneous transluminal coronary angioplasty

Percutaneous transluminal coronary angioplasty (PTCA) was performed unsuccessfully, resulting in disruption and near-total closure of the proximal right coronary artery at the site of stenosis following balloon inflation. The artery could not be reopened in the catheterization laboratory despite intracoronary nitroglycerin, sublingual nifedipine, and multiple balloon inflations. Myocardial revascularization surgery was immediately performed with excellent graft flow. No apparent myocardial infarction resulted. Catheterization performed at one year showed normal left ventriculography, total occlusion of the bypass graft, and reopening and normalization of the right coronary artery at the site of PTCA-induced occlusion. Possible mechanisms for this phenomenon and its clinical implications are discussed.     

Case of angina pectoris at rest and during effort due to coronary spasm and myocardial bridging

We present a case of a 71-year-old male who had chest symptoms at rest and during effort. He had felt chest oppression during effort for 1 year, and his chest symptoms had recently worsened. One month before admission he felt chest squeezing at rest in the early morning. He presented at our institution to evaluate his chest symptoms. Electrocardiography and echocardiography failed to show any specific changes. Because of the possibility that his chest symptoms were due to myocardial ischemia, he was admitted to our institution for coronary angiography (CAG). An initial CAG showed mild atherosclerotic changes in the proximal segment of the left anterior descending coronary artery (LAD) and mid-segment of the left circumflex coronary artery. Subsequent spasm provocation testing using acetylcholine revealed a bilateral coronary vasospasm, which was relieved after the intracoronary infusion of nitroglycerin. Finally, a CAG showed myocardial bridging (MB) of the mid-distal segments of the LAD. Fractional flow reserve using the intravenous administration of adenosine triphosphate was positive at 0.77, which jumped up to 0.90 through the myocardial bridging segments when the pressure wire was pulled back. Thus, coronary vasospasm and MB might have contributed to his chest symptoms at rest and during effort. Interventional cardiologists should consider the presence of MB as a potential cause of myocardial ischemia.     

Acute ST-segment elevation myocardial infarction: A rare initial presentation of previously undiagnosed essential thrombocythemia

Essential thrombocythemia (ET) is a myeloproliferative disorder characterized by hemorrhagic and thrombotic complications. We describe a rare case of ST-segment elevation myocardial infarction (STEMI) in a patient with previously undiagnosed ET, confirmed by gene mutation. A 68-year-old man presented with severe acute chest pain and was diagnosed with STEMI. Primary coronary angiography showed severe stenosis with thrombus in the proximal left anterior descending coronary artery. Percutaneous aspiration thrombectomy was performed with no residual stenosis. The patient was discharged on antiplatelet agents, aspirin, and clopidogrel. Further investigations for intracoronary thrombus with no underlying atherosclerotic disease revealed positive Janus kinase 2 (JAK2) V617F gene mutation, and this was consistent with a diagnosis of ET with elevated platelet count. This case describes a rare initial presentation of previously undiagnosed ET with acute STEMI and highlights the potential importance of secondary workup for non-atherosclerotic causes of STEMI with isolated intracoronary thrombus otherwise normal coronary vasculature with no focal atherosclerosis.     

Acute ST-segment elevation myocardial infarction: A rare initial presentation of previously undiagnosed essential thrombocythemia

Essential thrombocythemia (ET) is a myeloproliferative disorder characterized by hemorrhagic and thrombotic complications. We describe a rare case of ST-segment elevation myocardial infarction (STEMI) in a patient with previously undiagnosed ET, confirmed by gene mutation. A 68-year-old man presented with severe acute chest pain and was diagnosed with STEMI. Primary coronary angiography showed severe stenosis with thrombus in the proximal left anterior descending coronary artery. Percutaneous aspiration thrombectomy was performed with no residual stenosis. The patient was discharged on antiplatelet agents, aspirin, and clopidogrel. Further investigations for intracoronary thrombus with no underlying atherosclerotic disease revealed positive Janus kinase 2 (JAK2) V617F gene mutation, and this was consistent with a diagnosis of ET with elevated platelet count. This case describes a rare initial presentation of previously undiagnosed ET with acute STEMI and highlights the potential importance of secondary workup for non-atherosclerotic causes of STEMI with isolated intracoronary thrombus otherwise normal coronary vasculature with no focal atherosclerosis.     

Vasospastic coronary occlusion associated with a myocardial bridge

A 53-year-old woman was admitted with unstable angina. Acute coronary angiography showed myocardial bridging and total occlusion of the left anterior descending artery in the middle one-third of its course. The occlusion was completely relieved by intracoronary administration of nitroglycerin. The occurrence of coronary spasm may explain angina and myocardial infarction in symptomatic patients with myocardial bridges.     

The effects of pretreatment with nitroglycerin on ischemic left ventricular dysfunction during coronary angioplasty

To evaluate the degree to which nitroglycerin reduces myocardial ischemia and dysfunction induced by transient coronary occlusion, 19 patients were studied during coronary angioplasty of the left anterior descending coronary artery. After a control occlusion of 60 seconds, 0.2 mg nitroglycerin was administered intravenously and the occlusion was repeated for 60 seconds. Before and during the occlusion period, pulmonary capillary wedge pressure was measured, the intracoronary ECG was recorded, and ventricular volumes, ejection fraction, and regional systolic shortening were obtained by digital subtraction angiography. Nitroglycerin caused a significant fall in pulmonary capillary wedge pressure before (10 vs. 7 mmHg) and at 60 seconds occlusion (18 vs. 14 mmHg), but did not significantly delay the rise in wedge pressure (37 vs. 44 seconds). End-systolic left ventricular volume at 60 seconds of occlusion was reduced by nitroglycerin (77 vs. 68 ml), whereas regional shortening of the ischemic segments remained unchanged (22 vs. 23%). Nitroglycerin did not delay the onset of ischemic ST-segment elevation (14 vs. 14 seconds) and had no effect on the changes of ST elevation in the intracoronary ECG (1.9 vs. 1.9 mV). These findings suggest that intravenous nitroglycerin reduces filling pressure and slightly improves left ventricular global function during acute coronary occlusion. Nitroglycerin, however, has little effect on ischemia-induced regional dysfunction and on ST-segment elevation in the intracoronary ECG.     

Vasospastic angina in a patient with hyperthyroidism

A 56-year-old man presented with typical angina pectoris lasting >20?min associated with precordial ST-segment elevation. Urgent coronary angiography showed critical stenosis in the proximal segment of the left anterior descending artery, which resolved with intracoronary nitrate application. He was subsequently diagnosed with hyperthyroidism secondary to exposure of iodinated contrast agent which is thought to be the cause of the coronary spasm. Symptoms resolved upon treatment with propylthiouracil, slow-release diltiazem, isosorbide mononitrate, and aspirin. This unusual case highlights the importance of considering hyperthyroidism in the differential diagnosis of chest pain and coronary artery spasm. We suggest routine thyroid function testing in patients with coronary spasm.     

Coronary artery spasm immediately after percutaneous transluminal coronary recanalization

A 55-year-old man developed acute inferior myocardial infarction. A coronary arteriogram performed within two hours later showed complete occlusion of the right coronary artery, which was not resolved by two doses of 300 micrograms of intracoronary nitroglycerin. It was recanalized with 50% luminal diameter narrowing after 600,000 units of urokinase. Immediately after this thrombolytic therapy, the patient experienced chest pain, and the coronary artery became completely obstructed again. The pain was promptly relieved by 300 micrograms of intracoronary nitroglycerin, with disappearance of the obstruction. The observations during the procedure indicate that coronary artery spasm can occur after successful thrombolytic therapy on an occluded artery, inducing postinfarction angina, and might culminate in a second complete occlusion after percutaneous transluminal coronary recanalization.     

Nitroglycerin-induced coronary vasodilatory responses in patients during isometric handgrip exercise

Intracoronary nitroglycerin is frequently administered during invasive procedures such as coronary angioplasty or thrombolysis which may be associated with pain and sympathetic neural stimulation. Whether sympathetic-mediated reflex vasoconstriction interferes with nitroglycerin-induced augmentation of coronary blood flow is unknown. Therefore, coronary and systemic hemodynamics were measured in 19 patients during isometric handgrip exercise (3 min x 25% maximal effort), during intracoronary nitroglycerin, and during handgrip plus intracoronary nitroglycerin. Nine patients had no significant left anterior descending coronary artery stenosis (group 1) and ten patients had greater than 70% left anterior descending coronary artery stenosis (group 2). Handgrip exercise increased heart rate, mean arterial pressure, and coronary sinus and great vein flow 15% while increasing coronary resistance 10%. Intracoronary nitroglycerin (200 micrograms) reduced mean arterial pressure -4 +/- 6% and increased great cardiac vein flow 35-72%. Anterior left ventricular regional coronary flow responses to intracoronary nitroglycerin were unaffected by sympathetic stimulation for group 1. Group 2 had a greater increase in great vein flow with intracoronary nitroglycerin plus handgrip compared to nitroglycerin alone due to increased mean arterial pressure with no change in the great vein resistance. These data indicate that sympathetic stimulation does not alter the nitroglycerin-induced augmentation of coronary sinus and great vein blood flow in patients with and without significant left anterior descending coronary artery stenosis. In patients undergoing invasive interventions who may have increased circulating catecholamines, mild sympathetic (isometric) stimulation does not appear to interfere with the coronary vasodilatory responses to intracoronary nitroglycerin.     

Acute myocardial infarction following food-dependent exercise-induced anaphylaxis

A 70-year-old man with a history of food-dependent exercise-induced anaphylaxis (FDEIA) since age 50 was admitted to the emergency department with chest pain and urticaria caused by FDEIA. Coronary angiography revealed total occlusion of the proximal left anterior descending coronary artery. After thrombus aspiration, a bare metal stent was placed into the culprit lesion, resulting in no residual stenosis. Urticaria disappeared on the second hospital day. This is the first reported case, to our knowledge, in which acute myocardial infarction followed FDEIA. Physicians should be aware of acute myocardial infarction as a rare but potential complication of FDEIA.     

Coronary spasm-induced acute myocardial infarction associated with intracoronary thrombosis]

A 63-year-old man was admitted with an acute anteroseptal myocardial infarction. Coronary angiography performed 3 hours after the onset of chest pain revealed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with delayed filling and intraluminal thrombus distal to the stenosis. After the intracoronary injection of isosorbide dinitrate, the delayed filling disappeared and a subsequent intracoronary urokinase partially dissolved the thrombus. Repeat coronary angiography in the chronic phase disclosed 75% stenosis of the LAD and disappearance of the thrombus. Intracoronary acetylcholine provoked a coronary spasm at the stenotic site of the LAD, concomitantly with chest pain and ST-segment elevation in the anterior leads. The present case demonstrated that coronary spasm plays an important role in thrombus formation and acute myocardial infarction. To date, the concept has been postulated that a dynamic interaction between atherosclerosis, platelet aggregation and spasm may work to cause coronary thrombosis and subsequently lead to acute myocardial infarction. Our report shed light on the importance of coronary spasm in the pathogenesis of myocardial infarction.