Spontaneous dissection of the LAD mimicking inferior myocardial infarction.

The case presented here is intended to raise awareness of two uncommon coronary angiographic findings in the clinical context of acute coronary syndrome. The prevalence of patients presenting with spontaneous coronary dissection as the underlying cause of an ST-elevation myocardial infarction is low. It is typically found in women, often occurring during the peripartum period. There is some debate as to whether spontaneous dissection could also be managed conservatively without coronary intervention. As for spontaneous dissection, knowledge of a culprit lesion within the distal left anterior descending artery (LAD) causing inferior ST elevation (wrap around of the LAD) is not prevalent. Patient characteristics and treatment options are discussed on the basis of the recent literature on both clinical entities.

Postcardiac injury syndrome following radiofrequeny ablation of atrial flutter.

We report the case of a 64-year-old woman who was admitted to our hospital for radiofrequency ablation of isthmus-dependent counterclockwise atrial flutter. Following an initially uncomplicated right atrial linear isthmus ablation that was associated with conversion of atrial flutter to sinus rhythm and evidence of complete isthmus block, the patient developed a small pericardial effusion, a marked and recurrent left-sided pleural effusion, and had significantly elevated inflammatory markers. After an extensive diagnostic work-up which excluded infectious, malignant and thromboembolic causes of the effusions, a diagnosis of postcardiac injury syndrome was made and the patient was treated with oral corticosteroids and nonsteroidal anti-inflammatory drugs. Over a treatment period of 2 months there was complete resolution of the pericardial and left-sided pleural effusions and normalization of inflammatory markers. Postcardiac injury syndrome is a rare complication of radiofrequency ablation that is characterized by signs of pericardial, pleural and pulmonary parenchymal inflammation.

Acquired right coronary artery fistula draining to the right ventricle: angiographic documentation of first appearance following reperfusion after acute myocardial infarction, with subsequent spontaneous closure.

Most coronary artery fistulae are congenital in origin but have been reported to be acquired as complications of chest trauma, coronary angioplasty, or rupture of a coronary artery aneurysm. This is the first angiographic documentation of a coronary fistula acquired after myocardial infarction that subsequently closed spontaneously during follow up.

Specific impairment of human platelet P2Y(AC) ADP receptor-mediated signaling by the antiplatelet drug clopidogrel.

Clopidogrel is an effective new antiplatelet agent useful for the treatment of ischemic cerebrovascular, cardiac, and peripheral arterial disease. However, the mechanism of clopidogrel action is not well understood, although it is known to inhibit ADP-evoked platelet aggregation. In the current study, the effect of clopidogrel on recently identified human platelet ADP receptors and their signaling pathways was investigated by using platelets from clopidogrel-treated subjects, 6 healthy volunteers (2 females and 4 males) who received 75 mg of clopidogrel daily for 7 days. Blood was taken and various platelet receptor signaling pathways were analyzed before treatment, after 7 days of medication, and 4 weeks after treatment had ceased. Platelet tests included the analysis of aggregation, rapid calcium influx, calcium mobilization from intracellular stores, adenylyl cyclase, and phosphorylation of vasodilator-stimulated phosphoprotein (VASP). The data indicate that clopidogrel does not affect those platelet ADP receptors coupled to cation influx (P2X1 ADP receptors) or calcium mobilization (P2Y1 ADP receptors). In contrast, clopidogrel treatment specifically impairs the ADP receptor coupled to G(i)/adenylyl cyclase (P2Y(AC) ADP receptors). Clopidogrel abolishes the inhibitory P2Y(AC) receptor-mediated ADP effects on prostaglandin E(1)-stimulated, cAMP-dependent phosphorylation of VASP without affecting epinephrine, thrombin, and thromboxane signaling. VASP phosphorylation is known to be closely correlated with the inhibition of platelet and fibrinogen receptor (glycoprotein IIb/IIIa) activation. Therefore, inhibition of the platelet P2Y(AC) ADP receptor and its intracellular signaling, including decreased VASP phosphorylation, is suggested as a molecular mechanism of clopidogrel action.

Intralobar lung sequestration with systemic coronary arterial supply.

Pulmonary sequestration is a rare anomaly. An accurate pre-operative evaluation of its vascular supply is essential for the surgeon's operative approach. We describe here an intrapulmonary sequestration with vascular arterial supply via the left circumflex and the right coronary artery. This case demonstrates that if aortography is unrevealing, then a coronary source should be considered in the preoperative search for the arterial supply to a pulmonary sequestration. Moreover, pulmonary sequestration should be listed in the differential diagnosis of aberrant coronary arteries.

Ligand specificity and ticlopidine effects distinguish three human platelet ADP receptors.

Human platelets express adenosine 5'-diphosphate (ADP)-specific purinoceptors of the P2X and P2Y receptor superfamily, but their structure, diversity, and precise pharmacological profile is not well understood. Here, functional assays with intact platelets and well-characterized nucleotide derivatives were performed in order to characterize the ligand specificity of these platelet-specific purinoceptors. For the signalling pathways investigated (aggregation, rapid Ca2+-influx, desensitization of Ca2+-influx, Ca2+-mobilization, inhibition of adenylyl cyclase), significant differences in ligand specificity were demonstrated. ADP activated all purinoceptors of human platelets, while adenosine 5'-triphosphate (ATP) was a weak agonist for the P2X receptor and an antagonist for the P2Y receptors. The ADP-receptor pathway-antagonist ticlopidine inhibited ADP-evoked aggregation and adenylyl cyclase inhibition but did not affect platelet purinoceptors associated with Ca2+-influx and Ca2+-mobilization. These results indicate the presence of three distinct ADP-selective purinoceptors on human platelets.

[Elective coronary implantation of a newly developed stent without conventional anticoagulation]. / Elektive koronare Implantation eines neu entwickelten Stents ohne klassische Antikoagulation.

OBJECTIVE: To assess in an open prospective study the angiographic and clinical results of the elective implantation of the recently developed AVE micro-stent (Applied Vascular Engineering, Santa Rosa, CA, USA), in combination with dual antiaggregation treatment. PATIENTS AND METHODS: Between January and December 1995 AVE micro-stents were implanted into 128 vessels in 121 patients (20 women, 101 men; mean age 60.7 +/- 9.5 [34-84] years) with symptomatic coronary heart disease (CHD). Indication for the primary implantation of the stent type was a complex morphology of the stenosis with unfavourable short- and long-term prognosis. The stent consists of a 4 mm long tubular highly flexible segment made of 0.008 inch wire and can be advanced even into tortuous vessels. After balloon dilatation of the stenosis the stent was advanced into the vessel wall at a pressure of 10-12 bar, followed by further dilatation at 16-18 bar. Conventional long-term anticoagulation was dispensed with, patients only receiving antiaggregation medication: 500 mg ticlopidine and 100 mg aspirin daily for 6 weeks. RESULTS: The primary success rate of stent implantation was 99% (121 of 122). Neither acute nor subacute thromboses were revealed during hospital stay nor was there any emergency bypass operation or early repeat balloon angioplasty. There were no abnormal bleedings. CONCLUSION: Stenoses which are unsuitable for conventional balloon angioplasty can be reliably treated with the AVE microstent. Optimal high-pressure dilatation in combination with dual antiaggregation treatment will prevent stent thrombosis and bleeding complications.

Platelet-vessel wall interactions, focal adhesions, and the mechanism of action of endothelial factors.

Endothelial cells produce a variety of vasoactive substances including prostacyclin (PGI2) and endothelium-derived relaxing factor (EDRF/NO) which are potent inhibitors of platelet adhesion/aggregation and vascular smooth muscle cell contraction/proliferation. PGI2 and EDRF elevate cAMP or cGMP, respectively, in vascular cells and other targets. The intracellular effects of cAMP and cGMP in vascular smooth muscle cells and platelets are primarily mediated by the family of cAMP- and cGMP-dependent protein kinases and their substrates. Important effector systems include enzymes, channels and regulatory proteins responsible for the regulation of intracellular Ca++. Other evidence suggests that VASP, a focal adhesion protein phosphorylated in platelets and smooth muscle cells in response to PGI2 and EDRF, is important for the regulation of integrins and cell-matrix interactions.