Cardiogenic shock and coronary endothelial dysfunction predict cardiac allograft vasculopathy after heart transplantation

Cardiac allograft vasculopathy remains one of the major causes of death post‐heart transplantation. Its etiology is multifactorial and prevention is challenging. The aim of this study was to prospectively determine factors related to cardiac allograft vasculopathy after heart transplantation. This research was planned on 179 patients submitted to heart transplant. Performance of an early coronary angiography with endothelial function evaluation was scheduled at three‐month post‐transplant. Patients underwent a second coronary angiography after five‐yr follow‐up. At the 5‐ ± 2‐yr follow‐up, 43% of the patients had developed cardiac allograft vasculopathy (severe in 26% of them). Three independent predictors of cardiac allograft vasculopathy were identified: cardiogenic shock at the time of the transplant operation (OR: 6.49; 95% CI: 1.86–22.7, p = 0.003); early coronary endothelial dysfunction (OR: 3.9; 95% CI: 1.49–10.2, p = 0.006), and older donor age (OR: 1.05; 95% CI: 1.00–1.10, p = 0.044). Besides early endothelial coronary dysfunction and older donor age, a new predictor for development of cardiac allograft vasculopathy was identified: cardiogenic shock at the time of transplantation. In these high‐risk patient subgroups, preventive measures (treatment of cardiovascular risk factors, use of novel immunosuppressive agents such as mTOR inhibitors) should be earlier and much more aggressive.     

Thoracic and cardiovascular interventions after orthotopic heart transplantation.

BACKGROUND: The long-term outcome of orthotopic heart transplantation is limited by the development of cardiac allograft vasculopathy, rejection, infection, and malignancy. METHODS: After heart transplantation, we treated patients with thoracic and cardiovascular diseases: preexisting coronary artery sclerosis in 2 patients, cardiac allograft vasculopathy in 19, valvular disease in 3, mycotic ascending aortic aneurysm in 2, superior vena cava stenosis in 2, and lung neoplasm in 10 patients. RESULTS: We successfully performed coronary artery bypass grafting for preexisting coronary artery sclerosis, valve replacement for valvular disease, and patch enlargement for superior vena cava stenosis. Percutaneous transluminal coronary angioplasty for cardiac allograft vasculopathy achieved excellent initial results, but the incidence of restenosis was high (67%). One patient who underwent coronary artery bypass grafting for cardiac allograft vasculopathy died immediately after operation. Graft replacement was performed for mycotic aortic aneurysm, but 1 patient required reoperation because of recurrent aneurysm. The long-term survival rate in patients undergoing surgical resection for lung neoplasm was poor (50%). CONCLUSIONS: The need for thoracic and cardiovascular interventions in patients after heart transplantation was low (4.7%). Use of the appropriate procedures can improve the long-term survival after heart transplantation.     

HLA‐DRB1 Typing by Micro‐Bead Array Assay Identifies the Origin of Early Lymphoproliferative Disorder in a Heart Transplant Recipient

We report the case of a 68‐year‐old woman who underwent heart transplantation for hypertrophic cardiomyopathy. Two months after the transplant she developed mild fever and dyspnea with a marked drop in left ventricle ejection fraction of 31%. Coronary angiography was negative for cardiac allograft vasculopathy. Endomyocardial biopsy revealed ischemic damage with no evidence of acute cellular rejection, antibody‐mediated rejection or viral myocarditis. A neoplastic process was suspected even though full‐body computerized tomography was negative for malignancy. The patient died 4 months after transplantation. The autopsy showed acute antero‐septal myocardial infarction due to a nodular epicardial EBV‐related posttransplant lymphoproliferative disorder (PTLD) infiltrating the left anterior descending coronary artery with occlusive neoplastic thrombosis. We highlight two major aspects of this case: (1) the unusual occurrence of early PTLD involving the cardiac allograft and causing a fatal outcome, (2) the application of an immunological technique for HLA‐DRB1 typing to posttransplant paraffin‐embedded autopsy material to identify the recipient origin of this early malignancy, thus excluding a possible donor‐transmitted neoplasm.     

Endothelin in coronary endothelial dysfunction early after human heart transplantation.

BACKGROUND: Cytokines and growth factors released as part of the immune response to alloantigenic stimuli are capable of regulating endothelin-1 expression in the allograft. Endothelin plays a significant role as a modulator of coronary vascular reactivity in the early stages of atherosclerosis and may be important as a participant in and marker for cardiac allograft vasculopathy. METHODS: We characterized a possible relationship between morphological and functional coronary changes, transcardiac plasma endothelin level and myocardial endothelin-mRNA expression in 33 cardiac transplant recipients in the early, stable phase 5+/-3 months after orthotopic heart transplantation. Coronary microvascular function was determined as endothelium-dependent with acetylcholine and endothelium-independent with adenosine using intracoronary Doppler-FloWire. The percentage of the epicardial diameter changes was measured using quantitative coronary angiography. Intravascular ultrasound was performed to quantify intimal hyperplasia. Cardiac endothelin uptake or release was determined by measuring plasma endothelin levels in the coronary sinus and aorta. Myocardial endothelin-gene expression was determined using semiquantitative RT-PCR. RESULTS: The aortic endothelin levels were significantly increased in transplant recipients compared to nontransplanted patients (11.8+/-2.2 vs 7.2+/-0.9 fmol/mL; P < 0.001). Endothelin uptake was noticed in the majority of patients, and the amount of endothelin uptake was correlated to microvascular (r = 0.37; P < 0.05) and epicardial (r = 0.41; P < 0.03) endothelium-dependent vasodilatation. High mRNA signal intensity was associated with significantly reduced coronary flow response to acetylcholine compared to patients with low myocardial gene expression (coronary flow reserve 2.4+/-0.9 vs 3.4+/-0.8, respectively; P < 0.005). Morphological coronary changes early after transplantation were not correlated to endothelin plasma levels or myocardial gene expression. CONCLUSION: Coronary endothelial vasomotor dysfunction after cardiac transplantation is associated with an increased myocardial endothelin mRNA expression and decreased endothelin-uptake by the heart. We postulate that early activation in the endothelin system may have a pivotal role in the acceleration of the atherosclerotic process in transplant patients.     

Dobutamine stress echocardiography predicts cardiac events or death in asymptomatic patients long-term after heart transplantation: 4-year prospective evaluation.

BACKGROUND: Cardiac allograft vasculopathy (CAV) remains the major cause of death after cardiac transplantation during long-term follow-up. Nevertheless, annual angiographic evaluation is difficult to perform routinely. We evaluated the value of clinical risk factors and non-invasive testing for cardiac allograft vasculopathy in predicting cardiac events or death in asymptomatic patients with normal ventricular function during long-term follow-up after heart transplantation. METHODS: We studied 39 patients, mean aged 48 +/- 13 years, at 86 +/- 31 months after heart transplantation. Patients underwent thallium scintigraphy, treadmill stress testing, dobutamine stress echocardiography, and angiography to detect CAV. We prospectively observed all patients an additional 4 years for acute myocardial infarction, congestive heart failure, or death. RESULTS: Angiography detected CAV in 15 patients (38%). Three patients had acute myocardial infarction and another 7 had congestive heart failure, representing 25% of cardiac events during the study period. Nine deaths (23%) occurred during the same observation time. Univariate analysis showed that increased body mass index, positive dobutamine stress echocardiography results, and positive angiography results were associated significantly with cardiac events or death during follow-up. In the absence of coronary angiography, stepwise logistic regression identified positive dobutamine echocardiography results as the unique independent predictor of cardiac events (p = 0.001) or death (p = 0.002). CONCLUSION: Cardiac events and death after heart transplantation increased during long-term follow-up of this population. However, dobutamine stress echocardiography is well tolerated and, in the absence of routine angiographic evaluation, may be a strong predictor of these events.     

Drug-Eluting Balloons–A New Tool in the Treatment of Cardiac Allograft Vasculopathy: A Case Series

Percutaneous coronary intervention in patients with cardiac allograft vasculopathy is burdened with a lot of difficulties. Although they have allowed significant progress in comparison with plain balloon angioplasty and bare metal stents, drug-eluting stents have not fully overcome problems of diffuse lesions and small-vessel disease that are so common in transplant coronary artery disease. There is growing evidence that drug-eluting balloons might be a better choice for patients with small vessel atherosclerotic coronary disease and yet there is no experience with this technology in patients with cardiac allograft vasculopathy. Herein we report a case series of successful percutaneous coronary interventions in patients with cardiac allograft vasculopathy.     

Emergency cardiac surgery in patients with acute coronary syndromes: a review of the evidence and perioperative implications of medical and mechanical therapeutics

Patients with acute coronary syndromes who require emergency cardiac surgery present complex management challenges. The early administration of antiplatelet and antithrombotic drugs has improved overall survival for patients with acute myocardial infarction, but to achieve maximal benefit, these drugs are given before coronary anatomy is known and before the decision to perform percutaneous coronary interventions or surgical revascularization has been made. A major bleeding event secondary to these drugs is associated with a high rate of death in medically treated patients with acute coronary syndrome possibly because of subsequent withholding of antiplatelet and antithrombotic therapies that otherwise reduce the rate of death, stroke, or recurrent myocardial infarction. Whether the added risk of bleeding and blood transfusion in cardiac surgical patients receiving such potent antiplatelet or antithrombotic therapy before surgery specifically for acute coronary syndromes affects long-term mortality has not been clearly established. For patients who do proceed to surgery, strategies to minimize bleeding include stopping the anticoagulation therapy and considering platelet and/or coagulation factor transfusion and possibly recombinant-activated factor VIIa administration for refractory bleeding. Mechanical hemodynamic support has emerged as an important option for patients with acute coronary syndromes in cardiogenic shock. For these patients, perioperative considerations include maintaining appropriate anticoagulation, ensuring suitable device flow, and periodically verifying correct device placement. Data supporting the use of these devices are derived from small trials that did not address long-term postoperative outcomes. Future directions of research will seek to optimize the balance between reducing myocardial ischemic risk with antiplatelet and antithrombotics versus the higher rate perioperative bleeding by better risk stratifying surgical candidates and by assessing the effectiveness of newer reversible drugs. The effects of mechanical hemodynamic support on long-term patient outcomes need more stringent analysis.     

Concomitant intramyocardial and epicardial vasculitis in an autopsied heart allograft for cardiac rhabdomyosarcoma

Primary cardiac tumours are rare, with only one quarter of the patients being malignant. The vast majority of malignant neoplasms of the heart are sarcomas. We describe a patient of primary cardiac rhabdomyosarcoma presented as coronary artery disease and recurrent myocardial infarction. Histopathologic finding of the excised native heart revealed a high grade pleomorphic rhabdomyosarcoma in the myoepicardial portion of the anterior wall with rupture. The accompanying unusual feature was myocardial infarction because of tumour emboli of the left anterior descending and left circumflex coronary arteries. After transplantation, the patient developed mild to moderate acute cellular rejection of the transplanted heart on post-transplantation day 1, 8, and 44, respectively. Unfortunately, he expired on the post-transplantation day 47 because of acute rejection, presenting as concomitant intramyocardial and epicardial lymphocytic vasculitis and multifocal myocardial ischaemia. We found that this uncommon medial lymphocytic vasculitis lesion was mediated by T cells and also by antibody directly against smooth muscle cells of small arteries. The consequence of such immune response would be compromised myocardial oxygenation resulting in allograft failure.     

Relationship between bridging with ventricular assist device on rejection after heart transplantation.

BACKGROUND: Ventricular assist devices (VADs) are commonly used to bridge patients to heart transplantation. Recipients of VADs may develop anti-human histocompatibility leukocyte antigen antibodies, as reflected by elevated panel-reactive antibodies (PRA). The purpose of this study was to evaluate the relationship between bridging with VAD before heart transplantation and development of cellular rejection, humoral rejection, and allograft vasculopathy after transplantation. METHODS: Data on all patients who underwent cardiac transplantation between July 1994 and February 2001 at Rush Presbyterian St Luke's Medical Center were retrospectively reviewed. Data collected included sex, age, etiology of cardiomyopathy, percentage panel reactive antibodies (by cytotoxic method), type and duration of mechanical circulatory support, transfusion history, rejection history (both cellular and humoral) after cardiac transplantation, and development of allograft vasculopathy. Cellular rejection was treated when International Society of Heart and Lung and Transplantation Grade 2 or greater in the first 12 months after transplant and Grade 3 or greater after 12 months and treated with intensification of immunosuppression. Humoral rejection was defined clinically as allograft dysfunction by echocardiography without evidence of cellular rejection on endomyocardial biopsy or allograft vasculopathy. Allograft vasculopathy was defined by presence of any degree of luminal narrowing or pruning of distal vessels by coronary arteriography. Statistical analyses were performed by chi-square test, Fisher's exact test, and Wilcoxon rank sum test, as appropriate. RESULTS: Ninety-eight patients underwent cardiac transplantation during the study period (87 men, mean age 49 years, 46 ischemic etiology). Of these, 48 were bridged with HeartMate VAD (20 patients received vented electric device, 28 received pneumatic device). Nineteen percent of VAD patients had a peak pretransplant PRA > or =10% vs 2% of patients without VAD (p = 0.014). PRA > or =10%, use of VAD, or duration of VAD support did not predict development of humoral rejection. Use of VAD did not predict development of cellular rejection or allograft vasculopathy. VAD use was not associated with sudden death after heart transplantation. In the entire group of 98 patients, neither humoral nor cellular rejection predicted development of allograft vasculopathy. Longer ischemic time correlated with increased cellular rejection and humoral rejection after transplantation (p = 0.01). CONCLUSIONS: Some patients bridged to cardiac transplantation with VADs have increased PRA before heart transplantation, but this does not appear to translate into increased risk of either humoral or cellular rejection after transplantation or development of allograft vasculopathy as detected by coronary angiography.     

Is all intimal proliferation created equal in cardiac allograft vasculopathy? The quantity-quality paradox.

BACKGROUND: Pre-angiographic detection of intimal proliferation using intravascular ultrasound in heart transplant recipients has focused investigators' attention on the prognostic utility of such early information. Not all heart transplant recipients who exhibit a "prognostically relevant" threshold of severe (>0.5 mm) intimal thickening experience cardiac events. We sought to contrast clinical characteristics of heart transplant recipients who have prognostically relevant, severe intimal proliferation and who experience cardiac events with those who remain event free. METHODS: We prospectively followed an inception cohort of 54 consecutive heart transplant recipients with severe intimal proliferation (intimal thickness >0.5mm) of the coronary arteries after index intravascular ultrasound examination to assess the development of cardiac events (sudden cardiac death, myocardial infarction) and/or the necessity for coronary revascularization with percutaneous techniques (angioplasty, atherectomy, stent implantation) or surgical bypass. RESULTS: Based on the occurrence of adverse cardiac events during the subsequent 24 months, we divided the study cohort into 2 groups: Group 1 (no event, n = 33) and Group 2 (cardiac event, n = 21). Both groups demonstrated similar intimal thickness at the index ultrasound (Group 1, 0.89 +/- 0.27 mm, vs Group 2, 0.94 +/- 0.36 mm; p = not significant). Those with cardiac events were more likely than those without events to have hyperlipidemia, to have greater exposure to cumulative and average daily prednisone, and to exhibit greater average biopsy rejection scores at follow-up. CONCLUSIONS: These observations underscore the importance of the quality and not merely the quantity of intimal proliferation in determining occurrence of morbid cardiac events and further emphasize the interaction of immunologic and non-immunologic factors in determining event vulnerability in cardiac allograft vasculopathy.     

Dobutamine stress echocardiography in the assessment of cardiac allograft vasculopathy in asymptomatic recipients

PURPOSE: Cardiac allograft vasculopathy (CAV) is the most important cause of late mortality among cardiac allograft recipients. Dobutamine stress echocardiography (DSE) is considered a safe and cost-effective method to screen these patients who remain free of angina most of the time. We evaluated DSE results in a series of cardiac allograft recipients. METHODS: The DSE was performed on a yearly basis. From 2004 to 2006, twelve DSEs were performed on 8 patients, including 7 men, and overall mean age of 36 +/- 12 years. Dobutamine infusion begun at 5 microg/kg/min was titrated at 3-minute stages to 10, 20, 40, and 50 microg/kg/min to achieve the target heart rate. In addition, at every stage, we performed a 12-lead EKG, heart rate, and blood pressure recording. The DSE results were compared with coronary angiograms and endomyocardial biopsies. RESULTS: Two patients displayed mildly and 1 patient a severely abnormal DSE test. The severely abnormal DSE test was associated with severe coronary artery stenosis, including inexperiment of the left main coronary artery. The second patient with an abnormal DSE had contour irregularities and distal cut-off of the right coronary artery as well as 2R cellular rejection. The third patient had a normal angiogram and no rejection. None of the patients with normal DSE experienced a cardiac event, coronary lesions, or rejection. CONCLUSION: Use of DSE appears to be a sensitive method to detect CAV in asymptomatic recipients. However, mild wall motion abnormalities can be detected in patients without stenosing coronary lesions. The value of DSE in predicting CAV must be examined in larger series with long-terms of follow-up.     

Aortocoronary artery graft during early and late phases of acute myocardial infarction

From April, 1968, to August, 1972, 30 patients received one to three emergency saphenous vein grafts during acute myocardial infarction. In all but 1 patient, acute myocardial infarction occurred while the patients were in the hospital awaiting coronary angiography or myocardial revascularization.The patients were divided into two groups: those in the early and those in the late phases of acute myocardial infarction, depending on the time interval between the onset of chest pain and operation. Twenty-four patients (early phase) received grafts within 10 hours after the onset of infarction, and 18 of these 24 patients underwent operation within 4 hours after infarction. Two patients included in this group sustained myocardial infarctions in the operating room during elective myocardial revascularization procedures; another patient was brought to the operating room following cardiac arrest and was supported by internal cardiac massage throughout the opening of the chest and cardiac cannulation. Six patients (late phase) received grafts from three to fourteen days after acute infarction because of postinfarction angina. Only 1 patient was in cardiogenic shock prior to operation.Two patients, both from the early phase group, died in the postoperative period; and 1 patient died seven months postoperatively from a noncardiac cause. Twenty-five of 27 surviving patients became asymptomatic, and 2 patients continue to have mild angina (Functional Class II). Sixteen patients with 24 grafts were restudied in the postoperative period, and 22 of the grafts were found to be patent.This experience suggests that early operative intervention in acute myocardial infarction by the saphenous vein graft technique is beneficial to the patient. The rationale of revascularization in the early phase of acute myocardial infarction is to minimize the area of muscle necrosis by increasing perfusion to the ischemic myocardium around the infarct.     

Relationship among epicardial coronary disease, tissue myocardial perfusion, and survival in heart transplantation.

BACKGROUND: Cardiac allograft vasculopathy continues to represent the major limitation to long-term cardiac allograft survival. Routine angiography and intravascular ultrasound fall short in their ability to detect microcirculatory aberrations. Thrombolysis in myocardial infarction (TIMI) myocardial perfusion grades (TMPG) have been used as a measure of microvascular circulation in patients treated for acute myocardial infarction. We studied the correlation of epicardial coronary anatomy with microvascular flow as determined by TMPG and correlated it with patient outcome. METHODS: We enrolled 66 consecutive cardiac transplant recipients (49 men; mean age 52 +/- 13 years; range 15-70 years) undergoing surveillance coronary angiogram during a 9-month period. All angiograms were interpreted for epicardial coronary anatomy by an independent investigator. Another investigator, blinded for clinical data and angiogram interpretation, interpreted TMPGs. TMPG 0 was defined as no apparent tissue-level perfusion; TMPG 1 indicated presence of myocardial blush but no clearance from the microvasculature; TMPG 2 blush cleared slowly; and TMPG 3 indicated that blush began to clear during washout (blush is minimally persistent after 3 cardiac cycles of washout). Cardiac deaths served as the primary outcome variable. RESULTS: Fifty-eight of 66 patients had an abnormal TMPG. Mean TMPG in all these patients was 4.2 +/- 3 (normal is 9). Forty-four patients (Group A) with no angiographic coronary narrowing had TMPG 4.81 +/- 3.1, and 22 patients (Group B) with epicardial coronary narrowing 40% of lumen diameter had TMPG 3.0 +/- 2.5 (p = 0.007). There was no difference in TMPG related to the coronary territory involved. At a mean follow-up of 30 +/- 2.5 months, 6 (13.6%) of 44 patients in Group A had died, and 7 (31.8%) of 22 in Group B had died (p < 0.03). CONCLUSIONS: Microcirculatory aberrations as assessed by tissue TMPG is abnormal across all coronary territories in cardiac transplant recipients and associated with poor survival, suggesting a generalized microvascular involvement even in the presence of a normal angiogram. Patients with focal epicardial coronary narrowing have significantly greater decline in tissue perfusion, independent of the coronary territory involved, and exhibit poor survival compared with patients without epicardial coronary disease.     

Vascular brachytherapy for treatment of cardiac allograft vasculopathy.

A high restenosis rate often follows treatment of coronary stenoses in cardiac allograft vasculopathy. We report successful coronary brachytherapy of a second in-stent restenosis in a patient after heart transplantation.     

Fever,Malaise, and Dyspnea in a Diabetic Heart Transplant Patient: A Case Report

Patients with solid-organ transplants usually present at the emergency department with nonspecific symptoms. The physician should consider a great variety of syndromes and diseases, given the greater risk that solid-organ transplant patients carry because of immunosuppression and transplant-related conditions. Myocardial infarction caused by cardiac allograft vasculopathy must be always suspected and ruled out, even when initial symptoms do not orientate in that direction. We present a case that conjugates signs that can be present in different pathologies. It shows that fever is not always related to infection or rejection but could also appear in acute cardiac allograft vasculopathy. It emphasizes the need of a multi-disciplinary team led by a heart transplant specialist when dealing with this sort of clinical case.     

Acute myocardial infarction due to coronary artery spasm after caesarean section

We experienced acute myocardial infarction due to coronary artery spasm after caesarean section. A 41-year-old multigravida woman with no previous cardiac history or coronary risk factor developed acute myocardial infarction after caesarean section, and was successfully resuscitated with emergency percutaneous transluminal coronary angioplasty. Acute myocardial infarction during pregnancy and postpartum period is a rare event, but could be associated with high mortality if it occurs. It is necessary to consider the possibility of acute myocardial infarction and provide early diagnosis and treatment by multidisciplinary team when a pregnant woman complains of retrosternal chest pain.     

Acute coronary syndrome: Uncommon presentation of multiple endocrine neoplasia

IntroductionMyocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable atherosclerosis plaque. There is also the acute myocardial infarction with no evidence of relevant stenosis of the coronary artery, known as myocardial infarction with non-obstructive coronary arteries (MINOCA) such as Takotsubo, myocarditis and catecholamine induced cardiomyopathy. Pheochromocytoma is one of the causes of MINOCA. This association is rare but it may delay diagnosis and must be known in order to provide the best chance at early detection.This work has been reported in the line with the SCARE criteria.Presentation of the caseWe report a case of a 49 year-old man, admitted to our department for a recurrence of myocardial infarction with angiographically normal coronary arteries. During his hospitalization the patient complained of intestinal haemorrhage. The abdominal Computed tomographic scan revealed bilateral adrenal mass. The diagnosis of pheochromocytoma was made and confirmed by a high level of normetanephirnes and metanephrines.DiscussionThe coexistence of multiple endocrine neoplasia type 2 and myocardial infarction appears to be a rare association rather than a coincidence.ConclusionIn this case we highlight the importance of thorough history taking and investigation for the determining the aetiology of MINOCA. As a reversible cause of myocardial dysfunction, catecholamine-induced cardiomyopathy can occur as a feature of multiple endocrine neoplasia. The prognosis depends greatly on early diagnosis and prompt medical and surgical treatment, which are unfortunately often delayed because of the challenging diagnosis in many cases.     

Circulatory Assistance with a Cardiac Allograft after Exclusion of the Canine Left Ventricle

Cardiogenic shock after myocardial infarction still carries a high mortality despite use of intraaortic counterpulsation and early surgical revascularization. An experimental canine model of left ventricular exclusion and circulation support was developed by closing the mitral valve and by interposing “in series” a cardiac allograft between pulmonary and systemic circulations. This preparation was able to support the recipient circulation after cardiopulmonary bypass in 25 animals. In 16 dogs the graft sustained life for from 1 to 32 days.It is hypothesized that such left ventricular assistance could be used to maintain the life of patients in cardiogenic shock after myocardial infarction. By providing maximal left ventricular decompression and improvement of the native coronary perfusion, this method may reverse the metabolic imbalance responsible for extension of the infarction, thereby salvaging muscle that is in jeopardy but still viable.     

Myokardinfarkte in der Schwangerschaft

Up to now 136 cases of myocardial infarction during pregnancy have been reported, and angiography revealed normal findings in 47%. In these cases coronary spasms have been discussed as the major mechanism of the disease. In isolated cases coronary artery dissection may also present with a normal coronary angiography. The case of a 31-year-old pregnant women who developed myocardial infarction during a caesarean section under spinal anaesthesia gives rise to the assumption that an early stage of coronary artery disease may be the third cause that has to be considered. Probably as a consequence of phases of tachycardia and hypertension during the course of anaesthesia, the patient developed a myocardial infarction that she survived without sequelae. While coronary angiography showed normal coronary vessels, an intravascular ultrasound study (IVUS) demonstrated an atheroma in the left main coronary artery with a ruptured fibrous cap. Laboratory screening for risk factors of coronary artery disease (CAD) showed hypercholesterinemia, increased factor VII activity and hyperfibrinogenemia. Platelet aggregation was not inhibited by acetylsalicylic acid. It was pointed out recently that even in asymptomatic patients, plaques may be present in coronary vessels indicating an early stage of CAD that cannot be diagnosed by angiography. Plaque rupture is often triggered by hypertension and may lead to myocardial infarction, instable angina pectoris, or sudden ischemic death. As IVUS is a new diagnostic tool that allows diagnoses of even early stages of CAD we believe that myocardial infarction during pregnancy is more often caused by plaque rupture than may be expected according to the current literature.     

Coronary vasospasm following subarachnoid hemorrhage as a cause of stunned myocardium. Case report

A patient with subarachnoid hemorrhage was found to have electrocardiographic abnormalities resembling an acute myocardial infarction as well as left ventriculographic findings of cardiac dysfunction. These cardiac abnormalities resolved following surgical clipping of the aneurysm and the patient recovered well from the operation. She died 2 months later from cancer and a postmortem examination at that time revealed no evidence of myocardial necrosis. In this report, the authors discuss coronary vasospasm and reversible postischemic "stunned myocardium," a condition that has not been considered previously in relation to subarachnoid hemorrhage.