The Canadian journal of cardiology
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Comparative Study
Angiographic and clinical outcomes of bivalirudin versus heparin in patients with acute coronary syndrome undergoing percutaneous coronary intervention.
Heparin with adjunctive glycoprotein IIb/IIIa platelet receptor (GP IIb/IIIa) inhibitors has demonstrated its effectiveness in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). Bivalirudin, a direct thrombin inhibitor, has recently been shown to be an effective alternative for patients undergoing elective PCI. ⋯ In the high-risk cohort undergoing PCI, bivalirudin with provisional GP IIb/IIIa inhibitors achieved better angiographic results. Although not powered to show a difference, and while acknowledging that a selection bias could have affected the data, the present study showed that bivalirudin may be as clinically effective and safe as heparin with adjunctive GP IIb/IIIa inhibitors.
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Acute ST-elevation myocardial infarction in patients with normal coronary arteries has previously been described, but coronary angiography in these patients was performed after the acute phase of the infarction. It is possible that these patients did not have normal angiograms during the acute phase (transient coronary thrombosis or spasm were usually suspected to be the cause). Information on the prevalence of truly normal coronary angiograms during the acute phase of a suspected ST-elevation myocardial infarction is lacking. ⋯ The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.
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It has long been debated whether patients with atrial septal defect (ASD) Eisenmenger syndrome have idiopathic pulmonary arterial hypertension with an incidental ASD or severe pulmonary hypertension on the basis of their ASD shunt magnitude alone. ⋯ ASD Eisenmenger syndrome may occur without BMPR2 mutation. Whether shunt magnitude alone or in combination with yet another genetic mutation is responsible for the development of pulmonary hypertension in these patients remains to be determined.