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PubMed · 2688879

Cardiovascular intervention.

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R K Myler. 1989. Cardiovascular intervention.. https://pubmed.ncbi.nlm.nih.gov/2688879/

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Cardiogenic shock.

PURPOSE: To review the cause, epidemiology, pathophysiology, and treatment of cardiogenic shock. DATA SOURCES: A MEDLINE search of the English-language reports published between 1976 and 1998 and a manual search of bibliographies of relevant papers. STUDY SELECTION: Experimental, clinical, and basic research studies related to cardiogenic shock. DATA EXTRACTION: Data in selected articles were reviewed, and relevant clinical information was extracted. DATA SYNTHESIS: Cardiogenic shock is a state of inadequate tissue perfusion due to cardiac dysfunction, most commonly caused by acute myocardial infarction. Mortality rates for patients with cardiogenic shock remain frustratingly high, ranging from 50% to 80%. The pathophysiology of cardiogenic shock involves a downward spiral: Ischemia causes myocardial dysfunction, which, in turn, worsens ischemia. Areas of nonfunctional but viable (stunned or hibernating) myocardium can also contribute to the development of cardiogenic shock. The key to achieving a good outcome is an organized approach that includes rapid diagnosis and prompt initiation of therapy to maintain blood pressure and cardiac output. Expeditious coronary revascularization is crucial. When available, emergency cardiac catheterization and angioplasty seem to improve survival. More recent developments, such as placement of coronary stents and use of glycoprotein IIb/IIIa antagonists, are promising but have not yet been well studied in patients with cardiogenic shock. In hospitals without direct angioplasty capability, stabilization with intra-aortic balloon counterpulsation and thrombolysis followed by transfer to a tertiary care facility may be the best option. CONCLUSIONS: Improved understanding of the pathophysiology of shock and myocardial infarction has led to improved treatment. If cardiogenic shock is managed with rapid evaluation and prompt initiation of supportive measures and definitive therapy, outcomes can be improved.

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Noninvasive assessment of the infarct-related coronary artery blood flow velocity using phase-contrast magnetic resonance imaging after coronary angioplasty.

This study assesses infarct-related coronary artery blood flow velocity using phase-contrast magnetic resonance imaging (MRI) in patients with reperfused acute myocardial infarction (AMI) and compares these results with flow measurements obtained nonsimultaneously by intracoronary Doppler ultrasound. MRI examination was performed in 17 patients with AMI within 1 to 4 days (mean 2.5 days) after direct or rescue coronary angioplasty using a 0.014-in Doppler guidewire. MRI was performed on a 1.5-T clinical imager. The fast gradient echo segmented k-space phase-contrast pulse sequence was employed during breath-hold. The MRI and Doppler parameters of average peak velocity and maximum peak velocity were measured. Mean phase contrast MRI average peak velocity was 13.3+/-10.7 cm/s, and mean phase-contrast MRI maximum peak velocity was 27+/-16.6 cm/s. Mean Doppler average peak velocity was 17.1+/-5.1 cm/s, and mean Doppler maximum peak velocity was 35.5+/-10.1 cm/s. At the same anatomic levels, phase-contrast MRI average peak velocity correlated significantly to Doppler average peak velocity (r = 0.52; p<0.006) and Doppler maximum peak velocity (r = 0.42; p<0.03). Phase-contrast MRI velocity measurements were correlated with the same heterogeneity of Thrombolysis In Myocardial Infarction 3 flow velocity observed during Doppler examination. Thus, by comparing phase-contrast MRI with invasive intracoronary Doppler flow measurements, the measured MRI values showed significant correlation with Doppler data. Phase-contrast MRI has the potential to noninvasively quantify coronary flow velocity and to evaluate quality of reperfusion in patients with AMI after reperfused therapy.

Angioplasty, Balloon, Coronary