Infarction In Young Patients Research Articles

Myocardial infarction in young patients (≤35 years of age) with systemic lupus erythematosus: a case report and clinical analysis of the literature

The present study aims to report a-20-year old girl with systemic lupus erythematosus (SLE) who developed myocardial infarction (MI) and also aims to review acute myocardial infarction (AMI) in young SLE cases (< or =35 years) reported in the literature. We conducted a comprehensive review of the English literature from 1975 to 2006 to analyse data on MI in SLE patients who had developed AMI either at 35 or earlier. In 32 English articles, we identified 49 SLE patients, plus our case, with AMI. They consist of 41 female and nine male patients, their mean age being 24 +/- 6.4 years (range of 5-35). Disease duration varied between 0 and 13 years. The lag time between the onset of the SLE manifestations and development of AMI was 7.7 +/- 5.4 year (range of 1 month to 20.5 years). We divided the patients into three subgroups according to their coronary involvement type (Group I: normal coronary artery or coronary thrombosis (n = 16); Group II: coronary aneurysm/arteritis (n = 12); Group III: coronary atherosclerosis (n = 22)). The lag time between the onset of the SLE manifestations and development of MI in the subgroups showed variations: Group I < Group II < Group III. Both prevalence of renal involvement and steroid therapy were higher in patients with coronary atherosclerosis than were in Group I. There were one or more risk factors for atherosclerosis in 39 SLE patients. AMI in young SLE patients may be seen, albeit rare. We suggest that clinicians should have a low threshold for cardiac evaluation in patients with SLE. Also, traditional risk factors could be managed through preventive measures.

Acute myocardial infarction in young patients: the culprit is not always a ruptured atherosclerotic plaque

Acute myocardial infarction in young patients: the culprit is not always a ruptured atherosclerotic plaque

Myocardial infarction in young patients without coronary atherosclerosis: assume primary antiphospholipid syndrome until proved otherwise

The objective of this study was to highlight the need for investigation of antiphospholipid (aPL) antibodies in patients presenting with myocardial infarction (MI) and normal coronary arteries at angiography. We present five patients who were found to have had an MI without evidence of atherosclerosis. All had aPL antibodies and thus fulfilled the diagnosis of antiphospholipid syndrome (APS). Who did not have recurrent events on long-term anticoagulation maintaining an international normalised ratio of 3-4. This study suggests that APS is probably a major cause of MI in those with normal coronary arteries at angiography. It is an important diagnosis to make as they do not require anti-atherosclerotic treatment but appear, from this case series, to do well on high-dose warfarin. Further clinical studies are necessary to look at prevalence and best management in these patients.

Characteristics and Outcome of Acute Myocardial Infarction in Young Patients

Background: The objective was to analyze the incidence, risk factors, management, and complications of acute myocardial infarction (AMI) in the young patient in Spain. Methods: Clinical characteristics, treatment, and outcome were analyzed in patients younger than 45 years admitted with an AMI diagnosis to the Coronary Units of 58 Spanish hospitals from 15th May to 15th December 2000. Results: Six thousand two hundred and ten consecutive patients were registered, 7% out of them were <45 years old. Outcome was better in the younger group, with a lower mortality rate at 28 days (3.7 vs. 11.9%; p < 0.001), demonstrating that age <45 years is an independent protective factor for mortality (relative risk: 0.41; 95% CI: 0.23–0.73; p < 0.001). This difference remained at 1-year follow-up. Conclusions: AMI in young patients presents distinct clinical characteristics, a different treatment, management and outcome with respect to the older group.

ABCA1 polymorphisms and prognosis after myocardial infarction in young patients

High-density cholesterol (HDL) levels are affected by genetic influences and certain behaviors. Low levels of HDL-C are considered as an independent risk factor for premature coronary heart disease. In patients with Tangier disease, characterised by low HDL levels, mutations in the ATP binding cassette transporter have been described. We have analysed three polymorphisms of the ABCA1 gene (-477C/T, R219 K, and I883M) in a cohort of young male survivors of myocardial infarction in order to know their influence in long-term prognosis. In premature heart disease, knowing prognosis factors is specially relevant.

Drug-induced myocardial infarction in young patients: Report of two cases

Drug-induced myocardial infarction in young patients: Report of two cases

Acute myocardial infarction in young patients: nutritional status and biochemical factors

Purpose: The aim of this study was to establish whether nutritional status and biochemical factors, C-reactive protein (CRP), serum amyloid A (SAA) protein, serum iron (Fe) and fibrinogen at admission were different in patients with acute myocardial infarction (AMI) at a young age (<40 years) vs. those with AMI at an older age (>60 years). We also investigated whether during the stay in the hospital, the increase in acute-phase reactants was different in young vs. older subjects, and if dyslipidemic aspects were different between the two groups. Methods: The study population consisted of 40 patients, all males with a mean age of 36.7±1.16 years, admitted to our facility with AMI. The control group included 40 patients, all males, mean age of 66.3±4.24 years, with AMI. CRP, SAA, Fe and fibrinogen were determined at admission to the hospital and daily for 7 days in the two groups of patients. Results: In young patients the median value of the highest levels were 6.2 mg/l (range 0.7–27.30) for CRP, 13.22 mg/l (range 0.7–130) for SAA, 420 mg/dl (range 76–840) for fibrinogen and 49.1 gamma/ml (range 14–102) for Fe levels. In the older patients, the median value of the highest levels were 5.9 mg/l (range 0.6–28.30) for CRP, 12.12 mg/l (range 0.9–280) for SAA, 480 mg/dl (range 60–780) for fibrinogen and 47.1 gamma/ml (range 12–94) for Fe levels. Conclusions: In the present study, acute-phase reactants were quantitatively similar in young and old patients. On the contrary, nutritional status, homocysteine, LDL and triglycerides are significantly higher in young patients than in old patients.

Acute myocardial infarction in young patients: nutritional status and biochemical factors

Purpose: The aim of this study was to establish whether nutritional status and biochemical factors, C-reactive protein (CRP), serum amyloid A (SAA) protein, serum iron (Fe) and fibrinogen at admission were different in patients with acute myocardial infarction (AMI) at a young age (<40 years) vs. those with AMI at an older age (>60 years). We also investigated whether during the stay in the hospital, the increase in acute-phase reactants was different in young vs. older subjects, and if dyslipidemic aspects were different between the two groups. Methods: The study population consisted of 40 patients, all males with a mean age of 36.7±1.16 years, admitted to our facility with AMI. The control group included 40 patients, all males, mean age of 66.3±4.24 years, with AMI. CRP, SAA, Fe and fibrinogen were determined at admission to the hospital and daily for 7 days in the two groups of patients. Results: In young patients the median value of the highest levels were 6.2 mg/l (range 0.7–27.30) for CRP, 13.22 mg/l (range 0.7–130) for SAA, 420 mg/dl (range 76–840) for fibrinogen and 49.1 gamma/ml (range 14–102) for Fe levels. In the older patients, the median value of the highest levels were 5.9 mg/l (range 0.6–28.30) for CRP, 12.12 mg/l (range 0.9–280) for SAA, 480 mg/dl (range 60–780) for fibrinogen and 47.1 gamma/ml (range 12–94) for Fe levels. Conclusions: In the present study, acute-phase reactants were quantitatively similar in young and old patients. On the contrary, nutritional status, homocysteine, LDL and triglycerides are significantly higher in young patients than in old patients.

A common polymorphism in the annexin V Kozak sequence (−1C>T) increases translation efficiency and plasma levels of annexin V, and decreases the risk of myocardial infarction in young patients

AbstractAnnexin V has phospholipid-binding capacity and plays a potent antithrombotic role. Recently, a C to T transition has been described in the Kozak region of this gene, affecting the nucleotide preceding the initiation ATG codon. We have developed a simple method to detect this genetic change, showing by analysis of 580 Mediterranean white subjects that the −1C to T transition (−1C>T) is a common polymorphism (allele frequency, 0.121). This polymorphism is in linkage disequilibrium with a new C>G polymorphism located 27 bp downstream in intron 2. We show that −1C/C carriers presented significantly lower plasma levels of annexin V than −1C/T subjects (0.45 ± 0.20 ng/mL versus 0.73 ± 0.28 ng/mL, respectively;P = .02). In vitro transcription/translation experiments support that the −1T allele increases translation efficiency. The clinical relevance of the −1C>T change was investigated in consecutive patients with nontraumatic spontaneous intracranial hemorrhage (n = 225), deep venous thrombosis (n = 151), and coronary heart disease (n = 101). Finally, we also studied 166 survivors of an acute myocardial infarction occurring at age of 45 or less. This polymorphism seems to have a minor effect in bleeding disorders, but to play a protective role against early myocardial infarction, reducing by 2-fold the risk of developing the disease (P = .006; odds ratio, 0.51; 95% confidence interval, 0.30-0.85).

A common polymorphism in the annexin V Kozak sequence (−1C>T) increases translation efficiency and plasma levels of annexin V, and decreases the risk of myocardial infarction in young patients

Annexin V has phospholipid-binding capacity and plays a potent antithrombotic role. Recently, a C to T transition has been described in the Kozak region of this gene, affecting the nucleotide preceding the initiation ATG codon. We have developed a simple method to detect this genetic change, showing by analysis of 580 Mediterranean white subjects that the −1C to T transition (−1C&gt;T) is a common polymorphism (allele frequency, 0.121). This polymorphism is in linkage disequilibrium with a new C&gt;G polymorphism located 27 bp downstream in intron 2. We show that −1C/C carriers presented significantly lower plasma levels of annexin V than −1C/T subjects (0.45 ± 0.20 ng/mL versus 0.73 ± 0.28 ng/mL, respectively;P = .02). In vitro transcription/translation experiments support that the −1T allele increases translation efficiency. The clinical relevance of the −1C&gt;T change was investigated in consecutive patients with nontraumatic spontaneous intracranial hemorrhage (n = 225), deep venous thrombosis (n = 151), and coronary heart disease (n = 101). Finally, we also studied 166 survivors of an acute myocardial infarction occurring at age of 45 or less. This polymorphism seems to have a minor effect in bleeding disorders, but to play a protective role against early myocardial infarction, reducing by 2-fold the risk of developing the disease (P = .006; odds ratio, 0.51; 95% confidence interval, 0.30-0.85).

Outcome after acute myocardial infarction in young patients: analysis of the PAMI database

Outcome after acute myocardial infarction in young patients: analysis of the PAMI database

Genetic Risk Factors Associated with the Prognosis of Myocardial Infarction in Young Patients

Genetic Risk Factors Associated with the Prognosis of Myocardial Infarction in Young Patients -

A Transesophageal Echocardiographic Study on Risk Factors for Stroke in Elderly Patients With Atrial Fibrillation: A Comparison With Younger Patients

Study objectivesAtrial fibrillation (AF) becomes an increasingly important cause of stroke as patients get older. The aim of the study was to determine whether risk factors of cerebral embolism among elderly patients with AF differed from those of younger patients by using transesophageal echocardiography (TEE). Design and settingCross-sectional study at a university hospital. MethodsCardiovascular lesions with the potential for thromboembolism in patients with AF were investigated using TEE. Left atrial spontaneous echocardiographic contrast (SEC), peak flow velocity in the left atrial appendage (LAA-flow), and aortic atherosclerosis of the thoracic aorta were assessed in 67 elderly (≥ 70 years old) and 135 younger (< 70 years old) patients. All patients underwent either brain CT (n = 54) or MRI (n = 148) to assess presence of cerebral infarction. ResultsCerebral infarction due to embolism was noted in 113 patients with AF. There was a higher prevalence of cerebral embolism in elderly patients when compared with younger patients (78% vs 45%; p < 0.001). Cerebral embolism found in younger patients was associated with high grade of SEC and lower LAA-flow (p < 0.05). In addition to these TEE findings, aortic atherosclerosis was more severe in elderly patients with cerebral embolism than in those without cerebral embolism (p < 0.0001). By multivariate logistic analysis, LAA-flow was an independent predictor of cortical infarction in younger patients, but not in elderly patients, whereas aortic atherosclerosis was a useful marker in predicting embolic risk in elderly patients. ConclusionsTEE findings indicative of left atrial blood stasis were useful to identify the embolic risk of younger patients with AF, while atherosclerosis of the thoracic aorta appears to be an important marker for cerebral embolism in elderly patients.

TESTICULAR INFARCTION ASSOCIATED WITH PROTEIN S DEFICIENCY

Protein S deficiency is a rare inherited disease in which a defect in the natural coagulation inhibitor protein S predisposes patients to thrombosis. Manifestations of protein S deficiency commonly include superficial and deep venous thrombosis, and pulmonary embolism. Mesenteric, myocardial and cerebral infarctions have been reported less frequently. To our knowledge we report the first case of testicular infarction due to protein S deficiency which manifested as acute scrotal pain. Our case might indicate the need to extend the concept of classic risk factors for testicular infarction in young patients. CASE REPORT A 17-year-old man had protein S deficiency and was taking prophylactic warfarin anticoagulant therapy. He had had several episodes of lower leg deep vein thrombosis during the last 7 years. He was admitted to our hospital with multiple ulcerative wounds and a painful, erythematous and swollen lower left leg. Lower left abdominal cramping occurred followed by left scrotal pain and rapid swelling. Physical examination revealed a red, swollen and tender left testicle. Pain was exacerbated by lifting the testicle above the pubic symphysis. Urinalysis showed 25 to 50 red blood cells per high power field but no pyuria. White blood count was 13,530/mm. 3 (normal 4,000 to 10,000), prothrombin time 17.4 seconds (normal 10.7 to 13.0) and activated partial thromboplastin time 38.3 seconds (normal 25 to 33). Doppler ultrasonography revealed a swollen and heterogeneous texture of the left testis with no Doppler signal of blood flow (fig. 1). Exploratory surgery was performed since the possibility of testicular torsion could not be ruled out. The left testis was explored through a scrotal incision. On gross examination the testis and epididymis were edematous, congested and darkened but the spermatic cord was in the normal position without torsion. Therefore, left orchiectomy was performed. Hemorrhagic infarction was evident on pathological examination. Microscopic examination revealed that thrombosis of the spermatic artery had resulted in testicular infarction (fig. 2). DISCUSSION

Acute myocardial infarction in young patient probably due to Kawasaki disease

Although the clinical course of Kawasaki disease is self limiting, coronary aneurysm or myocardial disorders develop in about 20% of the patients. In recent years there have been reports of ischemic heart disease as sequelae of Kawasaki disease in adults, especially young adults. In Korea, there was only one case report in 1995. We report a young woman who presented as acute myocardial infarction with coronary artery aneurysms which highly suggest the underlying Kawasaki disease. The acute myocardial infarction in this patient seems to be the late cardiologic sequelae of Kawasaki disease, which has been silent clinically until the presentation as an acute myocardial infarction. New noninvasive diagnostic tests are being tried to improve the detection of coronary artery complication. However, coronary angiography is still widely used to determine the presence of coronary artery lesions and access the feasibility of coronary intervention. Another advantage of coronary angiography is that, it is possible to analyze the shape and the size of aneurysm and predict the prognosis. In this case we performed the percutaneous transluminal coronary angioplasty (PTCA) instead of surgery. Further study comparing surgery with percutaneous coronary angioplasty is needed. (Korean Circulation J 2001;31(1):119-124)

Glycoprotein Ia gene C807T polymorphism and risk for major adverse cardiac events within the first 30 days after coronary artery stenting

The glycoprotein complex Ia/IIa (GP Ia/IIa) is a major collagen receptor on platelets and other cell types. Recently, linked polymorphisms within the coding region of the GP Ia gene (C807T and G873A) were identified that are related to GP Ia/IIa surface expression. The T807/A873 allele is associated with high expression, whereas the C807/G873 allele is associated with low surface expression of GP Ia/IIa. Subsequently, the T807 allele was found to be associated with coronary and cerebral infarction in younger patients. Platelet adhesion to the vessel wall plays a pivotal role in thrombosis after coronary artery stent placement. The goal of this study was to test whether C807T polymorphism is associated with a higher incidence of thrombotic events following coronary stenting. Consecutive patients treated with coronary stent placement (n = 1797) were genotyped for C807T polymorphism with polymerase chain reaction and allele-specific fluorogenic probes. The composite end point was defined as death, myocardial infarction, or urgent target vessel revascularization within 30 days of stent implantation. The genotype distribution of the study population was CC in 36.5%, CT in 46.7%, and TT in 16.8% of the patients. The incidence of the composite end point was 6.5% in T allele carriers and 5.3% in noncarriers (odds ratio for T allele carriage 1.23 [95% confidence interval, 0.81-1.86],P = .33). After adjusting for other baseline characteristics, the odds ratio for the composite end point was 1.15 (0.76-1.75). Therefore, C807T genotype has no significant influence on the major adverse events occurring after coronary artery stenting.

Glycoprotein Ia gene C807T polymorphism and risk for major adverse cardiac events within the first 30 days after coronary artery stenting

AbstractThe glycoprotein complex Ia/IIa (GP Ia/IIa) is a major collagen receptor on platelets and other cell types. Recently, linked polymorphisms within the coding region of the GP Ia gene (C807T and G873A) were identified that are related to GP Ia/IIa surface expression. The T807/A873 allele is associated with high expression, whereas the C807/G873 allele is associated with low surface expression of GP Ia/IIa. Subsequently, the T807 allele was found to be associated with coronary and cerebral infarction in younger patients. Platelet adhesion to the vessel wall plays a pivotal role in thrombosis after coronary artery stent placement. The goal of this study was to test whether C807T polymorphism is associated with a higher incidence of thrombotic events following coronary stenting. Consecutive patients treated with coronary stent placement (n = 1797) were genotyped for C807T polymorphism with polymerase chain reaction and allele-specific fluorogenic probes. The composite end point was defined as death, myocardial infarction, or urgent target vessel revascularization within 30 days of stent implantation. The genotype distribution of the study population was CC in 36.5%, CT in 46.7%, and TT in 16.8% of the patients. The incidence of the composite end point was 6.5% in T allele carriers and 5.3% in noncarriers (odds ratio for T allele carriage 1.23 [95% confidence interval, 0.81-1.86],P = .33). After adjusting for other baseline characteristics, the odds ratio for the composite end point was 1.15 (0.76-1.75). Therefore, C807T genotype has no significant influence on the major adverse events occurring after coronary artery stenting.

Causes and Mechanisms of Cerebellar Infarction in Young Patients

To the Editor: The recent article by Barinagarrementeria and colleagues,1 dealing with the causes and mechanisms of cerebellar infarction in young patients, is not only informative but also provocative. The finding that 67% were caused by vertebral artery dissection raises several questions. Specifically, the pathogenesis of spontaneous vertebral artery dissection remains unknown, yet several independent factors exist that may provide clues. Did any of the individuals have chiropractic therapy,2 shampooing in a beauty parlor,3 or sustained neck angulation activity4 …

Abstracts of Literature

Abstracts of Literature

Causes and mechanisms of cerebellar infarction in young patients.

The incidence of cerebellar infarction in a series of patients with stroke is approximately 1.5%. The average patient age in most reported series is 62 years. The most common etiologies in this age group are atherosclerosis and cardiac embolism. The aim of this study was to determine the causes and mechanisms of cerebellar infarction in patients younger than 40 years. We analyzed retrospectively the clinical and radiological data from 21 men and 16 women with cerebellar infarction admitted to our hospital from January 1986 to December 1996. The patients had been studied extensively to determine the etiology of the cerebellar infarction. In the 37 patients (mean age, 30 years), 29 infarcts were limited to one territory (15 in the posteroinferior cerebellar artery [PICA]; 14 in the superior cerebellar artery); 8 had nonterritorial infarctions. The most common stroke mechanisms in each territory were as follows: PICA: nonatherosclerotic vasculopathic (67%), cardioembolic (20%), and hematologic and cryptogenic (each 7%); superior cerebellar artery: cardioembolic (42%), cryptogenic (31%), migrainous (21%), and nonatherosclerotic vasculopathic and hematologic (each 7%); and mixed territory: nonatherosclerotic vasculopathic (50%), cryptogenic (25%), cardioembolic (12%), and hematologic (12%). The most common mechanism of cerebellar infarctions was arterial occlusion as a result of intracranial vertebral artery dissection (40%), mainly with PICA involvement. Embolism from a cardiac source resulted primarily from patent foramen ovale and rheumatic valvular disease. Hematologic disturbances and migraine were responsible for a few cases.