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O Parodi

Publications and source records attributed to O Parodi.

At least 127 records · Page 7Linked to original sources

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.

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Coronary vasospasm in angina pectoris.

Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.

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Transient transmural reduction of myocardial blood flow demonstrated by thallium-201 scintigraphy, as a cause of variant angina.

In previous studies we demonstrated that variant angina could not be attributed to increased myocardial demands. In order to investigate whether a reduction of regional myocardial blood supply could be responsible for these ischemic episodes, we studied regional myocardial perfusion in six patients admitted to our coronary care unit. Myocardial scintigrams, obtained 5-7 min following i.v. injection of 1 mCi of thallium-201, performed during an episode of ST-segment elevation, showed transmural deficits of tracer uptake in the heart wall corresponding to the leads showing ST-segment elevation. These regional deficits ahd disappeared by 2 hours because of late uptake in previously ischemic myocardium. One week later, following injections performed in the absence of acute ischemia, no deficit was apparent. Tracer uptake in ischemic areas was 60% to 85% of that observed a week later. After adjusting for thallium-201 kinetics and counting geometry promblems., these scintigrams actually represent large underestimations of actual flow reduction. Thus variant angina appears to be caused by massive transmural reduction of myocardial blood supply.

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[Clinical coronarographic characteristics and pathogenetic mechanism of angina pectoris with s-t elevation (author's transl)].

The study of 46 patients with frequent anginal episodes characterized by S-T elevation (so called "variant angina pectoris") demonstrated that this type of electrocardiographic pattern does not characterize a homogeneous group of patients. In fact, while in some patients angina occurred only at rest, in others it occurred also on exercise. Sometimes ecgraphic alterations characterized by S-T depression were observed on the same leads which on other occasions had shown S-T elevation. The angiographic picture revealed: absence of significant coronary alterations in 10% of cases, stenosis greater than 75% in one main branch in 29%, in two branches in 39% and in three branches in 22% of cases. The hemodynamic monitoring carried out on 14 of these patients demonstrated that the ecgraphic modifications occur before the onset of the hemodynamic parameters which control myocardial O2 consumption. This suggests a primitive reduction of regional myocardial blood supply as a cause of the ischaemic episodes. The study of the regional myocardial perfusion with 201Tl technique in 6 patients confirmed this hypothesis. Coronary angiography carried out during an ischemic episode showed that the reduction of myocardial blood supply was caused by a spasm of a large coronary artery involving a long segment of the vessel, reversible by nitroglycerin administration. Aorto-coronary by-pass operation performed on 6 patients was followed by the disappearance of pain in two patients, even though the "by-pass" patency was angiographically proved in two patients.

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Myocardial cell damage during attacks of vasospastic angina in the absence of persistent electrocardiographic changes.

We have investigated whether vasospastic anginal attacks might be associated with myocardial cell damage even when permanent ORS or ST-T changes are absent. We obtained serum time-activity curves of creatine kinase MB, of myoglobin, and of alpha hydroxybutyrate dehydrogenase in 15 patients with vasospastic angina admitted to our Coronary Care Unit (CCU). A slight but consistent rise and fall of both myoglobin and creatine kinase MB was observed in 7 patients (4 presented a definitive myocardial uptake of 99mTc pyrophosphate, and I had a faint deposition). A similar pattern was observed for myoglobin alone in 3 patients (1 presented a negative myocardial scan), while no consistent changes were found in the remaining 5 patients (2 presented a faint deposition of 99mTc pyrophosphate). No significant change of alpha hydroxybutyrate dehydrogenase was observed in any of the patients. The coherent rise and fall of the levels of myocardial cytosolic components after prolonged episodes of vasospastic angina suggests that cell damage may occur even in the absence of persistent QRS and ST-T changes.

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Incremental diagnostic value of dipyridamole echocardiography and exercise thallium 201 scintigraphy in the assessment of presence and extent of coronary artery disease.

BACKGROUND: The incremental diagnostic information of two noninvasive tests for the detection of coronary artery disease (CAD), dipyridamole echocardiography, and exercise 201Tl myocardial scintigraphy was assessed in a series of 102 patients with ordered logistic regression and receiver-operating characteristic curves. METHODS AND RESULTS: Patients were selected from those referred to our cardiovascular centers with the clinical suspicion of CAD. After clinical evaluation, all patients underwent both noninvasive tests during hospitalization 2 weeks before coronary arteriography. The coronary arteriogram was used as a gold standard: CAD was defined as the presence of one or more vessels with 50% or greater narrowing of the luminal diameter. Clinical data were 73.0% +/- 5.7% accurate in the prediction of CAD. The addition of dipyridamole echocardiographic data to the clinical model yielded a diagnostic accuracy of 88.3% +/- 4.3% (p < 0.00001), whereas the addition of thallium scintigraphic parameters to the clinical model improved diagnostic accuracy to 93.8% +/- 2.6% (p < 0.00001). A significant increase in accuracy to 97.2% +/- 1.4% was achieved when thallium scintigraphic data were added to the clinical and dipyridamole-echocardiographic model (p < 0.00001). CONCLUSION: Both noninvasive methods for detection of CAD, DET, and ETS showed a good diagnostic accuracy especially when tests-derived parameters were combined with clinical data by means of relative logistic models; nevertheless the ETS model showed a higher sensitivity in comparison with the DET model, essentially in presence of a lower extent of CAD.

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Regional concordance and discordance between rest thallium 201 and sestamibi imaging for assessing tissue viability: comparison with postrevascularization functional recovery.

BACKGROUND: Whether the combined analysis of rest 201Tl and sestamibi uptake provides additional information regarding myocardial viability in patients with coronary artery disease is still to be investigated. METHODS AND RESULTS: To this aim we studied 22 patients with previous myocardial infarction and regional ventricular dysfunction by quantitative rest sestamibi and 201Tl scintigraphy. All patients underwent revascularization, and echocardiography was repeated 11 +/- 2 weeks later. Concordant results were obtained in 80 of 105 dyssynergic segments. Fifty-one segments showed normal and 29 abnormal activity. Follow-up echocardiography showed increased wall motion contractility in 76% of segments with maintained 201Tl and sestamibi uptake and in only 17% of segments characterized by subthreshold activities. Twenty-five segments, or 24%, showed sestamibi/201Tl mismatch. Eleven of 12 segments with normal sestamibi/abnormal 201Tl activity did not improve after revascularization, whereas 11 of 13 segments with abnormal sestamibi but normal 201Tl showed postoperative improvement of regional wall motion. CONCLUSIONS: In patients with previous myocardial infarction, sestamibi and 201Tl showed concordant results in most segments. However, in segments with mismatch a maintained sestamibi uptake was a poor indicator of tissue viability, whereas significant 201Tl uptake reflected tissue viability in most segments.

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