High impedance and low energy stimulation with bipolar ultrasmall electrode surface area steroid eluting lead (CapSure Z)

Thirty-five patients received a Capsure Z Medtronic bipolar model 5034 for the ventricle and 5534 for the atrium. These have 1.2 mm2 totally proprous, platinized, steroid eluting distal electrodes. The control group was repesented by 14 consective patients reciving CapSure SP medtronic model 5024 for the ventricle and 5524 for the atrium. At implant and during the follow-up period (6 months), CapSure Z and SP showed similar low pacing theresholds without early peaking in atrium (0.5 +/- 0.26 V vs 0 +/- 0.21 V at 0.5 msec P=NS., 0.06 +/- 0.01 msec at 1.6 V P=NS, respectively) and while Capsure Z showed a lewr value at six months in ventricle (0.3 +/- 0.1 V vs ).4 +/- 0.23 V P=NS, respectively) and while Capsure Z showed a lower value at six months in ventricle (0.3 +/- V vs 0.4 +/- 0.23 V P=NS at 0.5 msec, 0.07 +/- 0.03 msec. vs 0.1 +/- 0.02 msec. P<0.02 at 1.6V, repectively). P and R wave sensing of CapSure Z was better thant that of CapSure SP at implant (P wave + 5 +/- 2.5 mV vs 3.80 +/- 1.95 m;R wave = 15.2 +/- 6.4 mV vs 13.13 +/- 5.5 mV, respecitively) and during the follow-up period achieving statistical significance at the 6 th mont oly for P wave (P wave = 3.33 +/- 1.6 mV vs 2.61 +/- 1.05 mV P<0.05; R wave = 13.9 +/- 5.17 vs 10.8 +/- 5.75 mV, P=NS). CapSure Z atrial and ventricular pacing impedance were double than that of CapSure SP one at implant (atrium: 1050 +/- 214 vs 491 +/- 51; ventricle: 1296 +/- 236 vs 481 +/- 81, p< 0.0001) and during the follow-up period (atrium: 1081 +/- 185vs553 +/- 60; ventricle 1186 +/- 256 vs 656+/- 68, P< 0.0001).

[The prognostic value of the ejection fraction at rest and under stress assessed by nuclear angiography in myocardial infarct patients]. / Valore prognostico della frazione di eiezione a riposo e da sforzo valutata mediante angiografia nucleare in pazienti con infarto del miocardio.

BACKGROUND: The aim of this study was to assess the utility of ejection fraction at rest (rEF) and its change during stress (delta EF) as a predictor of cardiac events during the follow-up of patients (pts) with myocardial infarction. METHODS: 74 pts (44 treated with thrombolytic therapy (TR), and 30 not (noTR)), were studied with 99mTcPYP angiography within 2 +/- 1 months, after AMI. By 20 +/- 10 months, 41 pts had no events (Group A) while 33 pts experienced cardiac events (3 deaths, 16 angina, 12 CABG, and 2 PTCA). RESULTS: rEF was similar in both Groups A and B (A 47 +/- 8 vs B 45 +/- 10 p. ns), 44 +/- 15 vs B-noTR 46 +/- 12 p. ns). delta EF was different between Groups A and B. Group A showed a positive delta EF (3.2 +/- 6), and this result was more evident in thrombolyzed AMI (A-TR 4.4 +/- 4.5 vs A-noTR 1.16 +/- 3.9 p. < 0.01). Group B showed a negative delta EF (-4.4 +/- 5.3), and this result was more evident in non thrombolyzed AMI (B-TR -2 +/- 6.4 vs B-noTR -5.8 +/- 8 p. < 0.01). CONCLUSIONS: A decrease in EF during exercise radionuclide angiography is useful in identifying pts with high risk of cardiac events after AMI. Thrombolytic therapy improves stress EF in both Groups A and B.

Usefulness of the dipyridamole-Doppler test for diagnosis of coronary artery disease.

Two-dimensional and Doppler echocardiographic studies and a hemodynamic investigation were performed during dipyridamole testing in 42 subjects (13 control subjects and 29 patients with coronary artery disease [CAD]), to evaluate the ability of dipyridamole Doppler echocardiography in identifying patients with ischemic left ventricular dysfunction. In the control group, after dipyridamole infusion, Doppler-derived parameters increased significantly from baseline (p less than 0.001). In patients with CAD, peak flow velocity, flow velocity integral and stroke volume failed to increase after dipyridamole infusion (0.89 +/- 0.21 to 0.85 +/- 0.18 m/s, difference not significant; 14 +/- 3 to 12 +/- 4 cm, difference not significant, and 56 +/- 13 to 50 +/- 14 ml/beat, p less than 0.05, respectively). Heart rate, rate pressure product, systemic vascular resistance and mean right atrial pressure had similar variations in the 2 groups. Changes in the 3 Doppler-derived parameters are closely related to the variations of peak positive dP/dt, stroke volume (thermodilution) and left ventricular end-diastolic pressure and are closely related to the coronary angiography jeopardy score and to the appearance of wall motion abnormalities. Thus, by combining Doppler and 2-dimensional echocardiography, dipyridamole-induced myocardial ischemia may be detected in a high percentage of CAD patients, providing a sensitive tool for identifying patients with high-risk coronary artery anatomy.

Painless versus painful myocardial ischemia: different left ventricular dysfunction detected by echocardiography.

The mechanism responsible for the absence of anginal pain in patients who have episodes of both painless and painful myocardial ischemia, still remains unknown. Does the pain depend on an overstimulation of receptive structures or is this symptom the product of the excitation of a well-defined receptive system? The aim of this work is to test the first hypothesis: whether silent attacks are accompanied by the same degree of mechanical impairment as symptomatic ones. The authors compared the echocardiographic left ventricular functional behavior in the same patient (6 patients) during painful and painless myocardial ischemia. The echocardiographic changes observed during silent ischemic attacks were significantly different from those detected during symptomatic attacks. The latter were characterized by a larger extension of the ischemic myocardium and, as a consequence, by a larger functional impairment. Symptomatic and asymptomatic ischemic attacks were recorded echocardiographically in the same patient during repeated attacks on the same day, and were always clearly differentiated by the degree of wall motion abnormalities. The echocardiographic monitoring during the ischemic attack seemed to confirm that the greater functional impairment preceded the onset of pain leading to the occurrence of this symptom. Nevertheless, it was impossible to identify a threshold value above which the ischemic attack will be symptomatic. Our data seem to indicate a close relationship between painful ischemia and a higher degree of ischemic damage. Thus, in patients with predominantly painful myocardial ischemia, the extension and the severity of ischemia could play an important role in determining this symptom.