In vivo imaging. Optical spectroscopy. Intravascular ultrasound. Near infrared spectroscopy. Data acquisition. Imaging spectroscopy. Show All Keywords.
The Vulnerable Atherosclerotic Plaque: Strategies for Diagnosis and Management
Dispersion based stimulated Raman scattering spectroscopy, holography, and optical coherence Anterior chamber blood cell differentiation using spectroscopic optical coherence tomography Proceedings of SPIE February 18 Detection and characterization of atherosclerotic plaques by Raman probe spectroscopy Interferometric near infrared spectroscopy iNIRS at short source detector separations Subscribe to Digital Library.
Killip T Kimball JT. Treatment of myocardial infarction in a coronary care unit. A two year experience with patients.
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Angiographic thrombus burden classification in patients with ST-segment elevation myocardial infarction treated with percutaneous coronary intervention. J Invasive Cardiol. Clinical and procedural predictors of no-reflow phenomenon after primary percutaneous coronary interventions: experience at a single center. Circ J. Braunwald E.
Coronary plaque erosion: recognition and management. Plaque erosion. Boston MA: Blackwell Publishing ; p. In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical angiographical and intravascular optical coherence tomography study. Sci Rep. Neutrophil to lymphocyte ratio predicts short-and long-term mortality following revascularization therapy for ST elevation myocardial infarction. Prognostic value of neutrophil to lymphocyte ratio in patients presenting with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention.
Comparison of neutrophil-to-lymphocyte ratio and mean platelet volume in the prediction of adverse events after primary percutaneous coronary intervention in patients with ST-elevation myocardial infarction. Postepy Kardiol Interwencyjnej. Monocyte to high-density lipoprotein ratio as a new prognostic marker in patients with STEMI undergoing primary percutaneous coronary intervention.
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Biomechanics and inflammation in atherosclerotic plaque erosion and plaque rupture: implications for cardiovascular events in women. PLoS One. Morphological-biohumoral correlations in acute coronary syndromes: pathogenetic implications. Int J Cardiol. High levels of systemic myeloperoxidase are associated with coronary plaque erosion in patients with acute coronary syndromes: a clinicopathological study.
The Vulnerable Atherosclerotic Plaque: Strategies for Diagnosis and Management - Google книги
Angiographic stent thrombosis after routine use of drug-eluting stents in ST-segment elevation myocardial infarction: the importance of thrombus burden. Platelet activation: assessment and quantification. Consequently MI has been redefined to encompass any necrosis in the setting of myocardial ischemia by any of the following possible etiologies [ 3 , 8 , 13 ]:.
Type 2 MI : MI secondary to an increase in oxygen demand or decrease in supply. The myocardial necrosis results from causes other than coronary plaque instability [ 8 ]. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anemia, respiratory failure, hypotension and severe hypertension. In addition, in critically ill patients and in patients undergoing major non-cardiac surgery, myocardial necrosis may be related to injurious effects of pharmacological agents and toxins [ 9 ].
Type 3 MI : Sudden unexpected cardiac death before cardiac biomarkers obtained. Cardiovascular disease CVD is the number one cause of death worldwide, accounting for Coronary heart disease mortality is decreasing in many developed countries, but it is increasing in developing and transitional countries, partly as a result of increasing longevity, urbanization, and lifestyle changes. This is likely to be due to the advent of more sensitive assays for myocardial injury, earlier pharmacotherapy, and reperfusion and prevention of STEMI [ 13 , 18 ].
NSTEMI is a result of an acute imbalance between myocardial oxygen demand and supply, most commonly due to a reduction in myocardial perfusion. Type 1 MI is most commonly caused by a non-occlusive thrombus that develops in a disrupted atherosclerotic plaque, and leads to non-occlusive or near-complete thrombosis of a vessel supplying the myocardium.
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Plaque rupture usually occurs at the weakest and thinnest part of the atherosclerotic cap often at the shoulder region. Ruptured plaques contain large numbers of inflammatory cells including monocytes, macrophages, and T lymphocytes [ 19 , 20 ]. It is thought that the lack of ST elevation is because the infarct does not involve the full thickness of the myocardium not a transmural infarction.
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Patients presenting with chest pain or discomfort with suspected ACS require urgent evaluation. The clinical spectrum of NSTEMI may range from patients free of symptoms at presentation to individuals with ongoing ischemia, electrical or hemodynamic instability due to large myocardium in jeopardy or cardiac arrest secondary to malignant ventricular ischemia. Therefore, it is essential to establish if the patient has ACS and if so, what is the likelihood the patient will have adverse clinical event [ 1 ].
Physicians will need to stratify the patients according to their risk status and according to the initial risk assessment to choose an appropriate management strategy. The initial risk assessment includes the history, examination, ECG, and cardiac biomarkers [ 1 , 23 ]. Angina pectoris is a kind of pain described as a sensation of tightness, heaviness, aching, burning, pressure, or squeezing typically localized at the retrosternal region.
The pain can often radiate to the left arm but may also radiate to the lower jaw, neck, both arms, back, and epigastrium. It is associated with exertion or emotional stress and relieved by rest or administration of sublingual nitroglycerin [ 1 ]. In ACS patients other symptoms including sweating, nausea, abdominal pain, dyspnea and syncope may be present.
Atypical presentations are also possible and characterized by epigastric pain, indigestion-like symptoms and isolated dyspnea. Atypical complaints are more often observed in the elderly, in women and in patients with diabetes mellitus, chronic renal disease or dementia [ 24 , 25 ].
The relief of pain at rest increase the probability of myocardial ischemia while the relief of symptoms after nitrates administration is not specific for angina pectoris [ 25 ]. In patients presenting with suspected MI to the emergency department, overall, the diagnostic performance of chest pain characteristics for MI is limited [ 25 ]. Risk factors increase the likelihood of NSTEMI include: Older age, male gender, family history of CAD, diabetes, hyperlipidemia, hypertension, renal insufficiency, previous manifestation of CAD as well as peripheral or carotid artery disease.
Physical examination is frequently unremarkable in patients with suspected NSTEMI but may reveal HTN or hypotension, the presence of third and fourth heart sounds, and paradoxical splitting of the second heart sound. Cardiac auscultation may reveal a systolic murmur due to ischemic mitral regurgitation, which is associated with poor prognosis [ 26 ] or a mechanical complication i. Signs of heart failure raised jugular venous pressure, bilateral crepitation on auscultation of the lungs or cardiogenic shock may also be present, and these signify a worse prognosis.
ECG is critical for the diagnosis of STEMI as the cause for the chest pain, this has a tremendous therapeutic implication for the patient. Standard leads may be inconclusive in some patients and additional leads may be necessary e.
Diffuse precordial ST depression more pronounced in leads V4—V6 may indicate a culprit lesion located in the mid left anterior descending coronary artery, while changes more evident in leads V2—V3 may be more suggestive of a culprit lesion located in the left circumflex artery [ 29 ].
BUN and serum creatinine: creatinine clearance should be estimated in NSTEMI patients and the doses of renally cleared drugs should be adjusted appropriately. In chronic kidney disease patients undergoing angiography, iso-osmolar contrast agents may be preferred [ 1 , 15 ]. Liver function tests: useful if treatment with drugs that undergo hepatic metabolism is considered.
Measurement, preferably, high-sensitivity cardiac troponin, is mandatory in all patients with suspected NSTEMI [ 7 , 8 , 9 ]. In patients with suspected myocardial ischemia, a dynamic elevation of cardiac troponin above the 99th percentile of healthy individuals indicates MI. Cardiac troponin levels rise rapidly i. The use of high-sensitivity assays, has shortened the time interval to the second cardiac troponin, reduced substantially the delay to diagnosis, translating into shorter stays in the emergency department and lower costs [ 6 , 7 , 8 , 9 , 32 , 33 , 34 , 35 ].