Ischemic Heart Disease Syndrome Research Articles

Women have less severe and extensive coronary atherosclerosis in fatal cases of ischemic heart disease: An autopsy study

The study aims to evaluate sex differences in extent and severity of coronary artery disease (CAD) and myocardial findings at autopsy among young people with fatal ischemic heart disease (IHD). Women with acute coronary syndrome are less likely than men to display obstructive CAD at angiography. This suggests unique mechanisms of acute coronary syndrome exist in women or may reflect prehospital death of women with the most severe CAD. Reports of autopsies by the Office of the Chief Medical Examiner of New York City on people aged 21 to 54 years who died between January 1, 2006, and December 31, 2008, were reviewed. A total of 639 cases of death due to atherosclerotic or arteriosclerotic cardiovascular disease according to the medical examiner were analyzed. Significant CAD was defined as ≥75% cross-sectional area stenosis in an epicardial vessel or ≥50% left main. Women were less likely to have obstructive CAD (63% vs 77% of men, P = .002). There was pathologic evidence of myocardial infarction (MI) in 43% of cases, 17% of which had nonobstructive CAD. Frequency of MI did not vary by sex overall (38% of women vs 45% of men, P = .18) or among those without significant CAD (23% vs 29%, P = .45). Among young people determined at autopsy to have died of IHD, fewer women had obstructive CAD, consistent with angiographic data in other IHD syndromes. Pathologic evidence of MI may exist in the absence of obstructive CAD.

Effectiveness of cardioprotective medication in women with suspected ischemic heart disease syndrome: the NHLBI-sponsored women's ischemia synrome evaluation (WISE) study

Knowledge of the effectiveness of cardioprotective medication in women with suspected ischemia is hampered by limited clinical trial data and heterogeneous risk. We assessed the effectiveness of cardioprotective medical treatment in women while adjusting for disease severity determined by cardiovascular magnetic resonance imaging (CMRI).

Plaque rupture and consequent thromboses probably do not cause acute coronary syndromes

The objective of this communication is to provide evidence that the spasm of resistance vessel (S-RV) concept of ischemic heart disease (IHD) and other ischemic disorders provides a more consistent set of explanations for acute coronary syndromes than the accepted mechanism of plaque rupture and consequent thromboses. The concept avers that S-RV directly induces symptoms in the various syndromes of IHD, including acute coronary syndromes. The S-RV concept is considered to be an alternate paradigm to explain IHD, and interest only develops in such models when there is significant doubt about the validity of the accepted paradigm. This report is an update of a study reported in this Journal in 1999 and has 2 changes; evidence will be evaluated by formal verification/falsification (pass/fail) methods – the method used to evaluate paradigms, and this report focuses on the mechanism of acute coronary syndromes because of the importance of these syndromes. It is well accepted that acute coronary syndromes are due directly to plaque rupture/thromboses, and there is considerable evidence to support this obvious mechanism. In spite of the obviousness of this mechanism, the S-RV concept asserts that S-RV is a more rational mechanism to explain acute coronary syndromes. Consistent with this position, the results of the study favor the S-RV concept. The standard position was given 8 passes, 2 passes with associated possible limited failures, and 2 possible failures. In contrast, the S-RV concept was given 12 passes, and no failures. Hopefully, the results of this study, and other available information about the S-RV concept, will prompt interest in the concept – such as independent testing of its premises.

Recent advances in myocardial contrast echocardiography.

Myocardial contrast echocardiography (MCE) has undergone many advances in the past several years through remarkable developments in contrast agent and ultrasound equipment technology. Microbubble ultrasound contrast agents can now safely transit the pulmonary circulation to provide opacification of the left ventricular cavity, improved endocardial border definition, and detection of myocardial perfusion. The role of contrast echocardiography in enhancing technically difficult images is now well established in clinical practice, and has proven especially useful in the stress and intensive care unit settings. Major progress has been made in the application of MCE for myocardial perfusion assessment in acute and chronic ischemic heart disease syndromes, and comprises the focus of this review. Advances in novel applications of contrast echocardiography, including targeted delivery of genetic and pharmaceutical materials, have also occurred, but remain in a preclinical phase. In summary, the combination of recent innovations in ultrasound equipment, and microbubble acoustics, allows for exciting exploration of the expanding role of contrast echocardiography in clinical practice.

Human C-reactive protein (CRP) 1059G/C polymorphism.

We found a novel G-->C change at nucleotide 1059 within exon 2 of the CRP gene encoding the C-reactive protein. The CRP 1059G/C polymorphism could be detected by digestion with endonuclease MaeIII. The frequency of the CRP 1059C allele was 0.109 in Caucasians, but it was absent from Canadian Oji-Cree. Because of the importance of the CRP gene product in inflammation and its recent association with ischemic heart disease syndromes, this polymorphism may be useful in the association studies of atherosclerosis and its related phenotypes.

Cyclic flow variations in a conscious dog model of coronary artery stenoses and endothelial injury correlate with acute ischemic heart disease syndromes in humans

Objectives. The purpose of this study was to test the hypothesis that episodes of cyclic flow variations (CFVs) in conscious dogs with coronary stenoses and endothelial injury correlate with acute ischemic heart disease syndromes in humans.Background. Although the canine model with CFVs has proved to be a useful model of coronary thrombosis, whether CFVs progress to these syndromes has not been clearly described.Methods. Cyclic flow variations were produced by an external constrictor placed at the site of the left anterior descending coronary artery with injured endothelium. Blood flow in this artery and 24-h Holter electrocardiogram (ECG) were recorded during the 1st 5 postoperative days.Results. Of 41 dogs that underwent the initial operative procedure successfully, 29 developed an episode of CFVs. In five dogs in which CFVs persisted throughout the monitoring period, the left anterior descending coronary artery flow decreased until day 3 and thereafter increased through day 5. Transient coronary occlusion during CFVs induced ST segment changes that returned to baseline after reflow. In 12 dogs, CFVs progressed to persistent coronary occlusion, and histologic examination revealed thrombus formation at the stenotic site and evidence of myocardial infarction. Four of these 12 dogs died suddenly of ventricular arrhythmias during persistent coronary occlusion; another 5 dogs died of reperfusion arrhythmias during CFVs with no evidence of myocardial infarction.Conclusions. Conscious dogs with CFVs closely correlated with clinical acute ischemic heart disease syndromes, suggesting them to be a useful model for investigating the complex mechanisms of cellular interactions in the pathogenesis of these syndromes.

A model of cyclic flow variations using canine coronary artery: An experimental model for ischemic heart disease syndrome

A model of cyclic flow variations using canine coronary artery: An experimental model for ischemic heart disease syndrome

Mechanisms of action of the organic nitrates in the treatment of myocardial ischemia

Nitroglycerin and the long-acting nitrates are widely used in all of the anginal syndromes and have proven effectiveness in relieving or preventing myocardial ischemia. Recent developments into nitrate mechanisms of action provide new insights as to the many anti-ischemic effects of these agents. Important concepts relating to coronary arterial endothelial function are germane to nitrate therapy. Endothelial-derived relaxing factor (EDRF) is presently believed to be nitric oxide (NO), which exerts vasodilatory and/or antiplatelet actions by increasing intracellular cyclic guanosine monophosphate as a result of activation of the enzyme guanylate cyclase. In the setting of coronary atherosclerosis, or even hyperlipidemia without histologic vascular disease, endothelial dysfunction may be present, promoting a vasoconstrictor/proplatetet aggregatory milieu. Nitroglycerin and the organic nitrates are NO donors; NO is the final product of nitrate metabolism, and in the vascular smooth muscle NO induces relaxation, resulting in vasodilation of arteries and veins. In the presence of inadequate EDRF production and/or release, it appears that nitroglycerin may partially replenish EDRF-like activity. Nitrates have long been known to have major peripheral circulatory actions resulting in a marked decrease in cardiac work. Venodilation and arterial relaxation result in a decrease in intracardiac chamber size and pressures, with a resultant decrease in myocardial oxygen consumption. In addition, a variety of direct coronary circulatory actions of the nitrates have been documented. These include not only epicardial coronary artery dilation, but the prevention of coronary vasoconstriction, enhanced collateral flow, and coronary stenosis enlargement. Recent work suggests that the nitrates may also act by preventing distal coronary artery or collateral vasoconstriction, which can reduce blood flow downstream from a total coronary obstruction. Thus, there are many anti-ischemic mechanisms of action by which nitroglycerin and the organic nitrates may be beneficial in both acute and chronic ischemic heart disease syndromes. The unique salutory effects of the nitrates in subjects with left ventricular dysfunction or congestive heart failure make these drugs particularly attractive for patients with abnormal systolic function and intermittent myocardial ischemia. Finally, the emergent role of intravenous nitroglycerin in acute myocardial infarction offers new prospects that nitrate therapy may prove to be beneficial in acute myocardial infarction as well as postmyocardial infarction for the reduction of left ventricular remodeling.

The use of aspirin in ischemic heart disease.

WITHIN a decade of the isolation of salicylate in 1892, aspirin was introduced as an analgesic and antipyretic agent. In 1971, Vane described its inhibition of prostaglandin synthesis from arachidonate in homogenates of guinea pig lung,1 and Smith and Willis demonstrated that aspirin blocks the production of prostaglandin in human platelets.2 During the past decade, it has been shown that platelet aggregation and the formation of thrombi are pathophysiologically important in syndromes of ischemic heart disease. As a result, aspirin is widely used in patients with ischemic heart disease, and its use has recently been advocated in subjects without clinically . . .

Transcardiac serotonin concentration is increased in selected patients with limiting angina and complex coronary lesion morphology.

Serotonin is released by activated platelets and may act as a mediator to initiate or sustain certain unstable syndromes of ischemic heart disease in humans. To determine whether or not serotonin concentration increases across the coronary bed in patients with severe, limiting angina, we measured central aortic and coronary sinus serotonin concentrations by a sensitive radioenzymatic assay in 39 patients with coronary artery disease and 13 patients with minimal or no coronary artery lesions as detected by arteriography. Although no difference existed in the mean aortic or coronary sinus serotonin concentrations between these two groups, elevated coronary sinus serotonin concentrations were detected in 23% of those with coronary artery disease. The coronary sinus and aortic serotonin concentration difference was greater in patients with significant coronary artery disease (0.6 +/- 6.62 ng/ml) compared with patients without significant coronary artery disease (-5.6 +/- 10.32 ng/ml) (mean +/- SD) (p less than 0.05). Further analysis revealed that patients with eccentric, irregular coronary artery lesions or intraluminal filling defects had a significantly elevated coronary sinus and aortic serotonin difference (3.1 +/- 5.54 ng/ml) compared with those with smooth concentric lesions (-1.9 +/- 6.61 ng/ml) (p less than 0.02). These data suggest that serotonin is released into the coronary circulation of some patients with coronary artery disease, especially those with frequent angina and complex coronary lesions. Although serotonin may be released in some patients with coronary artery disease, the specific pathophysiologic role of serotonin in the development or perpetuation of certain coronary syndromes in humans remains to be determined.

Unstable Angina Associated with Factor VIII Concentrate Therapy for Hemophilia A

Brief Report1 August 1986Unstable Angina Associated with Factor VIII Concentrate Therapy for Hemophilia AROBERT G. KOPITSKY, M.D., EDWARD M. GELTMAN, M.D.ROBERT G. KOPITSKY, M.D.Search for more papers by this author, EDWARD M. GELTMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-2-215 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe importance of intracoronary thrombosis in patients with atherosclerotic coronary stenosis has been well established in the pathogenesis of acute transmural myocardial infarction (1). Recent angiographic studies have shown that intracoronary thrombi also occur in many patients who have unstable angina without myocardial infarction (2-5). In patients with severe atherosclerotic coronary obstruction, it is conceivable that a severe coagulation defect could partially protect against unstable angina or acute myocardial infarction by impairing the ability to form intracoronary thrombi; correction of the defect could negate this protection. We describe a case of severe unstable angina associated with the use of factor...References1 DEWOODSPORESNOTSKE MJR. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med. 1980;303:897-902. CrossrefMedlineGoogle Scholar2. HOLMESHARTZLERSMITHFUSTER DGHV. Coronary artery thrombosis in patients with unstable angina. Br Heart J. 1981; 45:411-6. CrossrefMedlineGoogle Scholar3. VETROVECLEINBACHGOLDCOWLEY GRHM. Intracoronary thrombolysis in syndromes of unstable ischemia: angiographic and clinical results. Am Heart J. 1982;104(4 pt 2):946-52. CrossrefMedlineGoogle Scholar4. MANDELKORNWOLFSINGH JNS. Intracoronary thrombus in nontransmural myocardial infarction and in unstable angina pectoris. Am J Cardiol. 1983;52:1-6. CrossrefMedlineGoogle Scholar5. ZACKISCHINGERAKERDINCERKENNEDY PTUBH. The occurrence of angiographically detected intracoronary thrombus in patients with unstable angina pectoris. Am Heart J. 1984;108:1408-12. CrossrefMedlineGoogle Scholar6. BUJAWILLERSON LJ. Clinicopathologic correlates of acute ischemic heart disease syndromes. Am J Cardiol. 1981;47:343-56. CrossrefMedlineGoogle Scholar7. GALLINOHAEBERLIBAURSTRAUB AAHP. Fibrin formation and platelet aggregation in patients with severe coronary artery disease: relationship with the degree of myocardial ischemia. Circulation. 1985;72:27-30. CrossrefMedlineGoogle Scholar8. OLIVA P. Unstable rest angina with ST-segment depression: pathophysiologic considerations and therapeutic implications. Ann Intern Med. 1984;100:424-40. LinkGoogle Scholar9. FUERTHMAHRER JP. Myocardial infarction after factor IX therapy. JAMA. 1981;245:1455-6. CrossrefMedlineGoogle Scholar10. SULLIVANPURDYBILLINGHAMGLADER DLMB. Fatal myocardial infarction following therapy with prothrombin complex concentrates in a young man with hemophilia A. Pediatrics. 1984;74:279-81. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ROBERT G. KOPITSKY, M.D.; EDWARD M. GELTMAN, M.D.Affiliations: Washington University School of Medicine St. Louis, Missouri PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byParadoxical thrombosis part 1: factor replacement therapy, inherited clotting factor deficiencies and prolonged APTTEndothelial dysfunction in haemophilia patientsClassic Polyarteritis Nodosa Presenting Rare Clinical Manifestations in a Patient with Hemophilia APotential role for rFVIIa in transfusion medicineAcute left anterior descending artery occlusion in a hemophiliac A patient during recombinant factor VIII infusion: Treatment with coronary angioplastySevere Haemophilia A Patient with Factor V Leiden Homozygosity Associated with Portal Vein Thrombosis and Myocardial InfarctionCerebral infarct associated with factor V Leiden mutation in a boy with hemophilia AFactor VIII, HIV and AIDS in haemophiliacs: an analysis of their relationshipAssociation of severe haemophilia A and factor V Leiden: report of three casesFatal complication of desmopressinFactor VIII, HIV and AIDS in haemophiliacs: An analysis of their relationshipDeep venous thrombosis in hemophilia A 1 August 1986Volume 105, Issue 2Page: 215-216KeywordsAcute myocardial infarctionCardiology and cardiovascular diseasesHemophilia AMyocardial infarctionPathogenesisStable coronary artery diseaseStenosisThrombosisUnstable angina ePublished: 1 December 2008 Issue Published: 1 August 1986 PDF downloadLoading ...

Calcium antagonists for acute ischemic heart disease

The pharmacologic and physiologic effects of the slow-channel calcium antagonists verapamil, nifedipine and diltiazem are reviewed. Relevant pathophysiologic features of various acute ischemic heart disease syndromes are also reviewed and the clinical applications of the slow-channel calcium antagonists to acute ischemic heart disease syndromes in patients are discussed.

Inpatient treatment of unstable angina: Clinical perspective and sequential management

In the last decade, increasing information has become available to the effect that an increase in coronary artery tone and coronary artery spasm play an important role in patients with various ischemic heart disease syndromes. Coronary spasm may be superimposed on a coronary vessel already severely obstructed by atherosclerosis. Conversely, spasm may occur in an artery that is only minimally involved with atherosclerosis. The majority of patients studied in the United States with both stable and unstable angina pectoris have underlying severe organic obstructive coronary artery disease. There has now emerged a considerable amount of information from several centers showing that the calcium-channel blockers or calcium-flux antagonists are highly effective in the treatment of stable and unstable angina pectoris. This report focuses on the uses and limitations of one of these agents, nifedipine, in patients with unstable angina and provides a sequential approach to their management.