Bernardino Tranchesi

Diagonal earlobe crease as a marker of the presence and extent of coronary atherosclerosis

This study evaluates the association between the presence of diagonal earlobe creases (ELC) and coronary artery disease (CAD). One thousand four hundred twenty-four patients (760 men and 664 women, aged 30 to 80 years) were examined for the presence of ELC and classified into 2 groups: group I control--1,086 consecutive patients who denied symptoms of myocardial ischemia and were admitted to a general hospital for other reasons; group II CAD--338 patients with documented CAD (presence of > or = 70% coronary diameter stenosis at angiography). ELC was present in 304 patients (28%) in group I and 220 (65%) in group II (p < 0.0001). The patients were stratified in age groups to isolate the influence of age because the prevalence of ELC and CAD increased with advancing age (p < 0.0001 for both). This association remained statistically significant in all decades, except for patients aged > 70 years. To further remove the confounding effect of different age and sex distributions between the groups, a direct adjustment of the ELC prevalence was performed. When adjusted for age and sex, the prevalence of creases was still 58% higher in patients with CAD than in control subjects (p < 0.001). The presence of ELC was also related to the extent of CAD as measured by the number of major arteries narrowed (p = 0.015). The observed sensitivity of the sign for the diagnosis of CAD was 65%, the specificity 72%, the positive predictive value 42% and the negative predictive value 87%.

Effect of combined administration of saruplase and single-chain alteplase on coronary recanalization in acute myocardial infarction

Abstract The effectiveness of recombinant single- or 2-chain tissue-type plasminogen activator (rt-PA, alteplase) l and single-chain glycosylated* and unglycosylated 3–5 urokinase-type plasminogen activator in promoting the recanalization of thrombosed coronary arteries in patients with acute myocardial infarction is well established. Because the intrinsic fibrin selectivity of these 2 plasminogen activators is mediated by different molecular mechanisms, 6,7 their combined effect on clot dissolution might be more than additive. Combinations of these drugs in animal models of thrombosis produced significantly greater lysis than could be explained on the basis of their additive effects. 8 In a pilot study in myocardial infarction, a relatively low dose of 2-chain alteplase and single-chain urokinase-type plasminogen activator given together induced recanalization of the occluded coronary in almost all patients. 9,10 We designed this trial to attempt to confirm these preliminary findings. Low doses of single-chain rt-PA and unglycosylated single-chain urokinase-type plasminogen activator (saruplase)-corresponding to approximately 20% and between 12 to 25%, respectively, of the currently recommended dose of each thrombolytic drug—were used.

Reperfusion arrhythmias in acute myocardial infarction — fact or coincidence?

Reperfusion arrhythmias were studied in a group of 20 patients submitted to coronary thrombolysis in the early hours of acute myocardial infarction. Arrhythmias were observed in 15 (75%) patients and consisted of ventricular arrhythmias and/or sinus bradycardia; 11/13 patients with reperfusion ventricular arrhythmias had the same type of arrhythmias before the procedure. This study group was compared to another group of 22 patients with acute myocardial infarction treated conventionally. There was no difference between both groups in regard to the incidence and type of ventricular arrhythmias. Sinus bradycardia only occurred during reperfusion in the study group and was significantly predominant in this group when compared with control group.

Long-term function in the remote region after myocardial infarction: importance of significant coronary stenoses in the non-infarct-related artery.

BACKGROUND--Left ventricular (LV) function is the most important determinant of outcome after a myocardial infarction. Global LV function after a myocardial infarction is affected not only by wall motion in the infarct zone but also by regional function in the contralateral territory. It was hypothesised that the presence of significant stenoses in coronary arteries supplying the contralateral territory might influence the ability of this region to compensate for damaged myocardium after a myocardial infarction. METHODS AND RESULTS--79 patients treated with thrombolysis for acute myocardial infarction had coronary and ventricular angiograms within 24 h and at a mean follow up of 12 months after myocardial infarction. Wall motion in the contralateral territory was analysed and scored by the centre line method and the change over time was correlated with the presence or absence of significant (> 70%) diameter stenoses in the non-infarct-related artery. Mean (SD) contralateral territory motion worsened, from 0.74 (1.78) to -1.55 (2.06) SD chord (p < 0.001) in 40 patients with stenoses, whereas contralateral territory motion improved from -0.02 (2.4) to 0.63 (2.21) SD chord (p < 0.05) in the 39 patients without coronary stenoses. The same pattern was present whether or not the infarct artery was patent. The global left ventricular ejection fraction at 12 months was also related to contralateral territory motion (r = 0.71, p < 0.001) and to the presence of coronary stenoses (54 (15)% in those with coronary stenoses and 62 (16)% in those without, p < 0.05). CONCLUSION--The results demonstrate that significant stenoses in arteries supplying the non-infarct territory adversely affect global and regional left ventricular function after a transmural infarction. Non-infarct artery anatomy should be considered in intervention strategies to improve left ventricular function after acute myocardial infarction.

Lipoprotein (a) levels do not influence the outcome of rt-PA therapy in acute myocardial infarction.

Lipoprotein (a) [Lp (a)] is highly atherogenic. Structurally, it closely resembles LDL, with an additional apolipoprotein, apo (a), which is covalently bound to apo B via disulfide bridges [101. Apo (a) has a remarkable homology with plasminogen, the zymogen of the primary thrombolytic enzyme, plasmin [7]. It has been postulated that, by molecular mimicry, Lp (a) could compete with plasminogen for cellular binding sites and thus thrombolysis would be inhibited [81. Plasminogen activators, such as rt-PA (recombinant tissue-type plasminogen activator) and streptokinase, are now routinely used within the first hours after myocardial infarction episodes in an attempt to dissolve thrombi and promote recanalization of the obstructed coronary artery. Karadi et al. [5] found that Lp (a) prolonged fibrinolysis time as challenged with streptokinase. Brown and Goldstein [1] in a study based on clinical data provided by other authors [4], suggested that high levels of Lp(a) could inhibit tissue plasminogen activator (t-PA) physiological functions leading to a higher reoccurrence of myocardial infarction. Indeed, Edelberg et al. [3] have recently showed in vitro that Lp (a) inhibits the activation of plasminogen by t-PA bound to fibrinogen fragments.