We investigated the hypothesis that a cardioprotective, antiarrhythmic effect might be obtained by brief ischemia of a remote part of the body before ischemia of the heart. Regional ischemia (RI) was induced in isolated Langendorff-perfused rat hearts: group I, 30-min RI and reperfusion (control hearts; n = 18); group II, 5-min RI before 30-min RI (a reference group of “classic” ischemic preconditioning; n = 12); and group III, ischemic preconditioning with in vivo 10-min limb ischemia (LI) before 30-min RI in the perfused heart ( n = 20). A significant decrease in reperfusion arrhythmia was found in groups II and III compared with group I ( P < 0.02). Release of norepinephrine (NE) and prostacyclin was higher in hearts from animals pretreated with LI ( P < 0.05). Prostacyclin increased in all groups at minute 1 of reperfusion, but there was no correlation to the antiarrhythmic effect. NE increased at the beginning of reperfusion after 30 min of ischemia; this release was significantly diminished after preconditioning with LI ( P < 0.05). We further investigated the role of NE in preconditioning with LI using drug interventions. Pretreatment with exogenous NE protected against tachyarrhythmia. Reserpine given 24 h before LI partially abolished the antiarrhythmic effect of LI preconditioning. However, the α1-adrenoreceptor blocker prazosin did not prevent the effect of LI preconditioning on either ischemic or reperfusion tachyarrhythmia. Therefore, brief ischemia of an extremity protects against reperfusion tachyarrhythmia. One of the humoral mediators involved in this response appears to be NE; others remain to be identified.

Background-The decay of the pressure gradient across a stenotic mitral valve is determined by the size of the orifice and net AV compliance (C n ). We have observed a group of symptomatic patients, usually in sinus rhythm, characterized by pulmonary hypertension (particularly during exercise) despite a relatively large mitral valve area by pressure half-time. We speculated that this discrepancy was due to low atrial compliance causing both pulmonary hypertension and a steep decay of the transmitral pressure gradient despite significant stenosis. We therefore tested the hypothesis that C n is an important physiological determinant of pulmonary artery pressure at rest and during exercise in mitral stenosis. Methods and Results-Twenty patients with mitral stenosis were examined by Doppler echocardiography. C n , calculated from the ratio of effective mitral valve area (continuity equation) and the E-wave downslope, ranged from 1.7 to 8.1 mL/mm Hg. Systolic pulmonary artery pressure (PAP) increased from 43Ϯ12 mm Hg at rest to 71Ϯ23 mm Hg (range, 40 to 110 mm Hg) during exercise. There was a particularly close correlation between C n and exercise PAP (rϭϪ0.85).Patients with a low compliance were more symptomatic (PϽ0.025). Catheter-and Doppler-derived values for C n , determined in 10 cases, correlated well (rϭ0.79). Conclusions-C n , which can be noninvasively assessed, is an important physiological determinant of PAP in mitral stenosis. Patients with low C n represent an important clinical entity, with symptoms corresponding to severe increases in PAP during stress echocardiography.

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Absence of early ST segment elevation resolution after angiographically successful primary PTCA identifies patients who are less likely to benefit from the early restoration of flow in the IRA, probably because of microvascular damage and subsequently less myocardial salvage.

This is a prospective study of 543 patients with stab wounds of the chest treated in a 15 month period. Four hundred and sixty-seven patients (86 per cent) were selected for conservative treatment with no mortality. Of the 76 patients in the operatively treated group 68 were operated on in the operating theatre with a mortality of 17 per cent, while the remaining eight had a thoracotomy in the resuscitation room with a mortality of 87.5 per cent. Indications for early operation would appear to be the presence of signs of cardiac or major vascular injury (i.e. tamponade, profuse bleeding, an absent or diminished peripheral pulse, and shock not responding to aggressive resuscitation). A cautious digital exploration of the chest wound may help identify these injuries by obtaining information about the knife tract (towards or away from the heart or major vessels). The presence of shock on admission should not be an absolute indication for operation. Half the 156 patients with shock on admission were treated conservatively with no mortality. The presence of a wound over the precordium is not in itself an absolute indication for surgery. Seventy-two such patients, including 14 with shock, were successfully treated non-operatively. Massive air leaks are usually self-controlled and none of the 24 such cases required operation. The amount or rate of blood loss via the thoracotomy tube is not a reliable index of the severity of the injury and it should not be a sole criterion for the selection of the type of treatment.

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ST segment elevation in leads V7 to V9 identifies patients with a larger inferior MI because of concomitant posterolateral involvement. Such patients might benefit more from thrombolytic therapy.