Successful recanalization of an occluded coronary artery by percutaneous coronary intervention, systemic administration of tirofiban, a glycoprotein IIb/IIIa inhibitor, and intracoronary thrombolysis with alteplase.

A 51 year-old male was admitted to our institution with subacute inferior myocardial infarction. Coronary angiography showed thrombotic occlusion of the right coronary artery. Percutaneous coronary intervention including the delivery of 3 stents was unsuccessful (TIMI grade 0 flow). In addition to an ongoing systemic administration of tirofiban, a glycoprotein IIb/IIIa inhibitor, the patient received intracoronary thrombolysis (ICT) with alteplase (recombinant tissue type plasminogen activator, rt-PA). There was complete reperfusion on control angiography the following day (TIMI grade 3 flow); 7 months later, there was still TIMI grade 3 flow. To our knowledge, this is the first report on systemic administration of tirofiban combined with ICT.

[Pilot study of the effectiveness of combination therapy with reduced dose alteplase and the glycoprotein IIb/IIIa antagonist tirofiban in acute myocardial infarct]. / Pilotstudie zur Wirksamkeit einer Kombinationstherapie einer reduzierten Dosis von Alteplase und dem Glykoprotein IIb/IIIa Antagonisten Tirofiban beim akuten Myokardinfarkt.

In a pilot study with a total of 43 patients (31 males, 12 females) at a mean age of 64.2 +/- 12.1 years, the efficacy of a combination of a reduced dosage of alteplase (50 mg) and tirofiban with a start infusion of 0.4 microgram/kg/min over half an hour and an infusion rate of 0.10 microgram/kg/min over 12 h (PRISM-PLUS, modified) in four patients and a bolus of 10 micrograms/kg over 3 minutes and an infusion rate of 0.15 microgram/kg/min over 24 h (RESTORE, modified) in 39 patients were tested in acute myocardial infarction with regard to patency of infarct vessel and TIMI flow according to coronary angiography after 60 minutes, 30-day mortality and bleeding complications. The use of tirofiban in the PRISM-PLUS dosage led to an infarct vessel patency of 25% with TIMI III flow in one case. There were no complications in the next 30 days in this group. The use of tirofiban in the RESTORE dosage led to an infarct-vessel patency of 87%, a TIMI III flow in 79%, a 30-day mortality of 2.6% and a slight PCI-associated bleeding complication in one case. The combination of alteplase in a reduced dosage and tirofiban with a single bolus and an infusion rate according to the RESTORE study with satisfactory efficacy and low complication rate seems to be useful in the management of acute myocardial infarction.

Valsartan for prevention of restenosis after stenting of type B2/C lesions: the VAL-PREST trial.

The following study was performed to evaluate the effects of chronic 6-month administration of the angiotensin I receptor antagonist valsartan on restenosis rate after stenting of type B2/C lesions in comparison to placebo. Despite encouraging results of the BENESTENT and STRESS trials, stenting of complex coronary lesions leads to an in-stent restenosis rate of up to 40%. Several attempts at systematic medical therapy (e.g., ACE inhibitors) have not improved these results. Because of the important role of angiotensin in endothelial function, the hypothesis that angiotensin I receptor antagonists after stent implantation lead to a reduction of the in-stent restenosis rate should be tested in a single-center trial. Two hundred and fifty patients with type B2/C coronary lesions were randomized in an open-label study with respect to age, gender, lesion type and indication of percutaneous coronary intervention to a chronic administration of 80 mg valsartan or placebo (beta-blocking agents and/or ACE inhibitors). In-stent restenosis rate according to quantitative coronary angiography (QCA) and need for reintervention as primary and secondary endpoints were analyzed after a repeat angiogram at 6 months in 99 patients with 80 mg valsartan and 101 patients with placebo. Chronic administration of 80 mg valsartan reduced the in-stent restenosis rate to 19.2% (n = 19/99) in comparison to placebo with an in-stent restenosis rate of 38.6% (n = 39/101) (p < 0.005). Reintervention rate was 28.7% (n = 29/101) in the placebo group and only 12.1% (n = 12) in the valsartan group (p < 0.005). QCA analysis of stented coronary segments disclosed no differences in reference vessel diameter (2.68 +/- 0.26 mm in the valsartan group versus 2.71 +/- 0.24 mm in the placebo group) but significant differences in stented vessel diameter (2.17 +/- 0.27 mm in the valsartan group and 1.60 +/- 0.20 mm in the placebo group) (p < 0.000001).

Familial hypertrophic cardiomyopathy associated with prolongation of the QT interval.

In a 61 year old female patient who suffered from atypical chest pain we diagnosed long QT syndrome by QTc duration of 467 ms, macroscopic T wave alternans and notched T waves in three leads and hypertrophic cardiomyopathy with asymmetric thickening of basal parts of the septum (2.0 cm) without relevant outflow tract obstruction by echocardiography. Coronary angiography could exclude coronary artery disease. In a systematic family screening two sons of the patient could also be diagnosed as having long QT syndrome with QTc durations of 472 and 496 ms and asymmetric septal thickening (1.8 and 2.1 cm, respectively). One of these two sons suffered from pre-syncope, the other was asymptomatic despite maximum sports activity. In the third son, LQTS and hypertrophic cardiomyopathy could be excluded.

[Fatal ventricular rupture after stent implantation in acute myocardial infarct with subsequent stent thrombosis: discussion of reperfusion injury as the cause]. / Tödliche Ventrikelruptur nach Stentimplantation im akuten Myokardinfarkt mit nachfolgender Stentthrombose: Diskussion eines Reperfusionsschadens als Ursache.

Ventricular rupture due to myocardial infarction is a well-known but rare complication. Since the introduction of thrombolytics or acute PTCA in the management of acute myocardial infarction, the frequency of this complication has further decreased. A case of lethal ventricular rupture in the course of acute stenting for myocardial infarction, acute stent thrombosis 7 hours after successful intervention, and successful reintervention with intracoronary administration of abciximab is reported. Myocardial rupture as a severe form of reperfusion injury is discussed.