Conversion factors of effective and equivalent organ doses with the air kerma area product in patients undergoing coronary angiography and percutaneous coronary interventions.

To derive effective dose (E), organ dose (HT) and conversion factors with the air kerma area product (KAP) in coronary angiography (CA) and percutaneous coronary intervention (PCI) by the radial route, using the ICRP 103 tissue weighting factors. The study included 34 patients referred for CA and 31 for PCI. E and HT were derived from in-the-field KAP measurements using Montecarlo methods. Median KAP of 23.2 and 56.8Gycm2 and E of 6.9 and 20.0mSv were found for CA and PCI, respectively. Mean KAP and E were significantly higher in males than in females (52.4±40.0 vs 32.3±16.6Gycm2; p=0.02) and (16.8±13.6 vs 10.7±5.8mSv; p=0.04). KAP (r=0.39; p=0.001) and E (r=0.34; p=0.005) showed a significant correlation with the patient's weight. Conversion factors between KAP and E (E/KAP) were 0.30±0.04mSvGy-1cm-2 for CA and 0.33±0.05mSvGy-1cm-2 for PCI. No significant differences in the E/KAP between males and females were found (0.31±0.05 vs 0.33±0.05; p=0.08). Again, no significant correlation was found between E/KAP and patient's weight (r=0.23; p=0.07). The correlation between E and KAP was excellent for CA (r=0.99) and PCI (r=0.96). The correlation between HT and KAP ranged from r=0.87 to r=1 and from r=0.71 to r=0.98 for CA and PCI, respectively. A single factor, the total KAP, could be used for a specific acquisition protocol to reliably estimate E and HT without the need of a patient's specific analysis. Conversion factors might be installation, X-ray beam quality or protocol dependent.

Detection of moderate and severe coronary artery stenosis with technetium-99m tetrofosmin myocardial single-photon emission tomography.

The aim of this study was to determine the diagnostic accuracy of technetium-99m tetrofosmin myocardial imaging for the localization of coronary artery stenoses of different degrees of severity. Stress-rest single-photon emission tomography (SPET) was performed on separate days in 80 patients (64 males, 16 females; mean age 61 years; 43 patients with previous myocardial infarction; 18 patients with pharmacological stress), within 6 months of coronary angiography. Scintigraphic images were blindly and independently evaluated by three observers. Coronary stenosis was defined as a >50% narrowing in luminal diameter; severe stenosis was defined as a proximal stenosis of >75% or a peripheral stenosis of >90%. Coronary angiography revealed normal coronary arteries or insignificant coronary stenosis in 13 patients and significant coronary stenoses in 67 patients. The sensitivity and specificity of 99mTc-tetrofosmin SPET in respect of severely stenosed vessels were, respectively, 80% and 65% for the left anterior descending artery (LAD), 100% and 46% for the right coronary artery (RCA) and 58 and 78% for the left circumflex artery (LCx) territories. Considering all the significantly stenosed vessels, a significant decrease in sensitivity was observed for LAD territories (to 59%, P=0.05), and a nonsignificant decrease for RCA (88%) and LCx (47%) territories while specificity values remained essentially unchanged. No significant changes in sensitivity or specificity were observed when regions with previous myocardial infarction were excluded. In conclusion, the sensitivity of 99mTc-tetrofosmin SPET for the localization of individual stenosed vessels is only moderate when all significant stenoses are considered, but the ability of this technique to predict the location of severe coronary artery stenoses seems satisfactory, with the exception of the low specificity in respect of RCA territories.

[Short and intermediate term clinical outcome in patients with cardiogenic shock treated with aortic counterpulsation]. / Evoluzione clinica a breve e medio termine di pazienti cardiopatici in shock cardiogeno trattati con contropulsazione aortica.

BACKGROUND: Despite improvements in coronary care, cardiogenic shock (CS) remains the leading cause of death in patients with dramatic cardiac diseases of which acute myocardial infarction (AMI) is the most frequent event. Conventional therapy for CS with coronary care unit (CCU) monitoring and vasopressor agents to support blood pressure has historically been associated with an 80% to 90% mortality rate in large series. Intra-aortic balloon pump (IABP) therapy for shock results in initial favourable clinical and haemodynamic responses, but ultimately, in most patients, death is merely delayed and hospital mortality still exceeds 80%. In several recent non-randomised series, coronary revascularisation performed early in the course of CS with the use of coronary artery by-pass grafting (CABG) or coronary angioplasty (PTCA) resulted in an apparent reduction in the hospital mortality rate to less than 50% in selected patients with shock. OBJECTIVES: This study reviews our experience of cardiogenic shock treatment at a time when standard care included aggressive use of the intra-aortic balloon pump counterpulsation, cardiac catheterisation, coronary angioplasty and/or coronary artery by-pass grafting, ventricular septal defect and mitral incompetence repair. METHODS: We retrospectively analysed 20 patients (13 M and 7 F, with an average age of 62 years and a half) affected by cardiogenic shock consecutively admitted to our CCU between October 1, 1992 and April 1, 1995. Fifteen patients (pts) were hospitalised for AMI, shock and pump failure (2 of them with pulmonary oedema), all with admittance delay less than 24 hours. Five patients were hospitalised for AMI with shock and mechanical defects, of which 3 pts with AMI and ventricular septal rupture and 2 pts with AMI and mitral regurgitation. All patients underwent IABP, coronary angiography (CA) and then were treated with PTCA, CABG and cardiac surgery or medical treatment. RESULTS: On the whole, 7 pts died (35%): 4 of shock, 1 of haemorrhagic complications, 1 of septic shock in the CCU, and 1 of heart failure after CABG in cardiosurgery. One more patient died of heart failure two months after discharge (late mortality 5%). Out of the 15 patients hospitalised with AMI, shock and pump failure, 13 patients with AMI and CS less than 24 hrs were treated as follows: 1 patient was successfully submitted to emergency CABG and 12 patients to PTCA of the infarct related artery (IRA). Eight patients enjoyed a good outcome, but 1 patient died of haemorrhagic complications and 4 with a persistently occluded IRA also died (3 in the CCU and 1 after CABG). Of the 2 remaining pts with AMI, shock and pulmonary oedema, 1 patient underwent CABG with success and 1 patient with the 3-vessel disease was submitted to PTCA with reperfusion of the IRA, but he died from reocclusion three days later. Out of the 5 patients with AMI, shock and mechanical defects, 3 patients with AMI and septal ventricular rupture underwent cardiac surgery and CABG with early and late success. One of the 2 patients with AMI, shock and mitral regurgitation underwent cardiac surgery with valve repair and CABG and had a good outcome, the other died from septic complications in the CCU. CONCLUSIONS: IABP is an useful device for stabilising patients in cardiogenic shock and safely performing angiography as well as PTCA, CABG or surgical correction of all mechanical complications with a more stable haemodynamic balance. Therefore, IABP is an useful tool to improve successful coronary revascularisation after direct PTCA or direct CABG. These data also suggest that the combination of successful coronary revascularisation and intra-aortic balloon pumping can improve survival in pts with cardiogenic shock complicating AMI with early pump failure.

Prognostic value of left ventricular mass in uncomplicated acute myocardial infarction and one-vessel coronary artery disease.

This study assesses the relative prognostic value of increased left ventricular (LV) mass compared with residual ischemic myocardium and angiographic characteristics of the diseased vessel in 76 patients with uncomplicated acute myocardial infarction associated with 1-vessel coronary artery disease (CAD). All patients underwent symptom-limited treadmill exercise testing, resting and dipyridamole echocardiography and coronary angiography before discharge, and were followed-up for 32 +/- 6 months. LV measurements were obtained in diastole according to the Penn convention. Measurements of LV mass were divided by body surface area to obtain LV mass index. A cut-off value of 135 g/m2 body surface area for men and 112 g/m2 for women was prospectively selected. The individual effects of clinical, stress testing and angiographic variables were evaluated by using the Cox regression model. Echocardiographic LV mass index was increased in 43 patients and normal in 33. There was no intergroup difference with respect to baseline clinical and angiographic variables, ejection fraction and prevalence of stress-induced ischemia. During follow-up there were 23 cardiac events in the 43 patients with increased LV mass index and only 5 in the 33 with normal LV mass index (p < 0.001). No patient died or had nonfatal reinfarction among patients with normal LV mass. Cox survival analysis identified an increased LV mass index as the only independent predictor of cardiac events (chi-square = 7.9; p < 0.005; RR = 5.4). Thus, these data suggest that LV mass is an important independent risk factor in patients with uncomplicated acute myocardial infarction associated with 1-vessel CAD.

Silent versus symptomatic dipyridamole-induced ischemia after myocardial infarction: clinical and prognostic significance.

The prevalence and prognostic significance of silent myocardial ischemia were prospectively assessed in 217 patients (mean age 57 +/- 9 years, 83% male) recovering from a first uncomplicated acute myocardial infarction and undergoing a dipyridamole echocardiography test before hospital discharge. Clinical, angiographic, exercise electrocardiographic (ECG) and dipyridamole echocardiographic variables were also examined. Of the 217 patients, 89 had no echocardiographically proved dyssynergy after dipyridamole, whereas 128 had dipyridamole-induced wall motion abnormalities that were silent in 94 (Group I) and symptomatic in 34 (Group II). There was no intergroup difference with respect to dipyridamole time (i.e., the time from onset of the test to frank dyssynergy: 7 +/- 3 vs. 8 +/- 3 min; p = NS); prevalence of inferior myocardial infarction (69% vs. 71%; p = NS); ischemic ECG changes during the test (83% vs. 71%; p = NS); diabetes (8.5% vs. 6%; p = NS); ongoing medical therapy; multivessel disease (57% vs. 56%; p = NS); and baseline left ventricular ejection fraction (57 +/- 13% vs. 57 +/- 10%; p = NS). There was also no significant difference between Group I and Group II with respect to wall motion score index at peak dipyridamole effect (1.77 +/- 0.39 vs. 1.78 +/- 0.36; p = NS). Patients were followed up for 24 +/- 4 and 25 +/- 5 months, respectively (p = NS). Life table analysis revealed no difference in unstable angina, reinfarction and death between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Dipyridamole echocardiography test. A new tool for detecting jeopardized myocardium after thrombolytic therapy.

BACKGROUND: We wished to assess whether dipyridamole echocardiography test (DET) can detect jeopardized myocardium after thrombolytic therapy. METHODS AND RESULTS: Seventy-six consecutive patients with a first acute myocardial infarction (AMI) were treated with 2 million IU urokinase i.v. within 4 hours of the onset of AMI and underwent high-dose (as much as 0.84 mg/kg over 10 minutes) DET 8-10 days after AMI. The results were correlated to the anatomy of the infarct-related vessel (IRV). In patients with positive DET, we evaluated the wall motion score index (WMSI; a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of interpreted segments. In a 13-segment model, each segment was assigned a score ranging from 1 (normal) to 4 (dyskinetic). Fifty-three patients had positive results on DET. Of these, 42 had dipyridamole-induced new wall motion abnormalities (WMAs) confined to the infarct zone or adjacent segments. In these patients, mean WMSI increased from 1.46 +/- 0.26 (at resting conditions) to 1.73 +/- 0.35 (at peak dipyridamole) (p less than 0.01), whereas no significant change was detected in negative patients (1.6 +/- 0.34 versus 1.57 +/- 0.34, p = NS). Coronary angiography showed a patent IRV (TIMI grade 2 or 3) in 53 patients and no or minimal reperfusion (TIMI grade 0 or 1) in 23 patients. A patent IRV with critical residual stenosis was found in 35 of 42 patients with dipyridamole-induced WMAs in the infarct zone and in 18 of 34 patients without WMAs (p less than 0.05). Among the 23 patients with occluded IRVs, nine had collateral flow to the distal vessel; six of these had a positive DET. Thus, the sensitivity and specificity for identifying a critically stenotic but patent IRV or the presence of a collateral-dependent zone were 66% and 93%, respectively. In a subset of nine patients with a positive DET in the infarct zone or adjacent segments, DET and a control coronary angiography were repeated 1-3 months after an angiographically successful (residual stenosis, 50% or less) coronary angioplasty in the IRV. The repeat DET was negative in eight patients (all with patent IRV at control angiography) and again positive in one patient, who showed restenosis at angiography. The WMSI, at resting conditions was similar before and after angioplasty, whereas it differed significantly at peak dipyridamole (1.7 +/- 0.2 versus 1.4 +/- 0.2, p less than 0.01). CONCLUSIONS: DET can identify the anatomy of the IRV, and dipyridamole-induced WMAs within the infarct zone detect regions with jeopardized myocardium that may benefit from intervention.

Stress testing in the period after infarction.

Dipyridamole echocardiography is gaining popularity as an exercise-independent diagnostic method in patients with suspected or demonstrable coronary artery disease. To assess its safety, feasibility, and diagnostic accuracy in patients recovering from uncomplicated acute myocardial infarction, 131 patients had the test before hospital discharge. The results were compared with those of maximum treadmill testing. We found that dipyridamole-induced transient asynergy remote from the infarct zone was more sensitive (74% versus 53%, p less than 0.05) and specific (97% versus 68%, p less than 0.01) than treadmill testing for detecting multivessel coronary artery disease. In a subgroup of 42 patients treated with thrombolytic therapy, dipyridamole echocardiography was able to detect in 27 the presence of jeopardized but viable myocardium in the infarct zone. An excellent correlation was found between dipyridamole echocardiography responses and infarct vessel patency. Finally, the prognostic impact of dipyridamole echocardiography on patients recovering from acute myocardial infarction was assessed in a consecutive series of 151 patients. Eighteen months of event-free survival was significantly different in patients with positive versus negative dipyridamole echocardiography results (76.1% versus 50.8%, p less than 0.01). The test was also superior to treadmill testing in predicting cardiac events. Thus, dipyridamole echocardiography performed early after acute myocardial infarction is safe, feasible, and accurate for predicting the extent of coronary artery disease and 18-month clinical outcome.

[The echo-dipyridamole test early after acute myocardial infarct: echocardiographic aspects and angiographic correlations]. / Il test eco-dipiridamolo subito dopo infarto miocardico acuto: aspetti ecocardiografici e correlazioni angiografiche.

To assess whether the different mechanical effects of intravenous dipyridamole were correlated with the location and distribution of the coronary arteries stenosis, 98 patients underwent high dose DET 8-10 days after an acute myocardial infarction. Left ventricular regional wall segments were identified in multiple views; a vascular territory was assigned to each coronary vessel. DET was positive in 68.4% of the patients (67/93), 59% (23/39) of those with single vessel disease, and 81% (44/54) of those with multivessel disease. Four different mechanical patterns of positivity of DET were observed: 1) marked worsening of wall motion in the same region showing asynergy (type I); 2) development of new wall motion abnormality adjacent to the infarct zone and located in the same vascular region (type II); 3) development of new wall motion abnormality adjacent to the infarct zone, but located in a different vascular region (type III); 4) development of transient remote asynergy (that is, a new wall motion abnormality in a region normal at rest and not directly adjacent to the infarct zone, type IV). Types I and II (asynergies in the infarct zone coronary bed) were found in patients both with single vessel disease or multivessel disease; by contrast, type III and IV were almost exclusively found in patients with multivessel disease (24/54 and 14/54 respectively) and occasionally in patients with single vessel disease (2/39 and 1/39 respectively). Thus, these two mechanical behaviours during dipyridamole infusion showed to be highly specific for predicting multivessel disease (95% and 97% respectively, sensitivity 44% and 26% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Early assessment of coronary artery bypass graft patency by high-dose dipyridamole echocardiography.

To assess the role of high-dose (up to 0.84 mg/kg during 10 minutes) dipyridamole echocardiographic testing in the evaluation of coronary artery bypass graft patency early after surgery, 18 consecutive patients with angina underwent dipyridamole echocardiography and coronary angiography before and 7 to 10 days after bypass surgery. Coronary angiography showed 2- or 3-vessel disease in 7 and 11 patients, respectively. A total of 53 bypass grafts were performed. Before bypass surgery 14 patients had a positive and 4 a negative test result. No complication occurred during the test performed early after surgery. Of the 14 patients with positive dipyridamole echocardiographic results before surgery, 10 had negative and 4 had positive results after surgery. All 4 patients had negative results before and after surgery. In the 4 patients with positive results after dipyridamole echocardiographic testing before and after bypass surgery, dipyridamole time increased from 5.8 +/- 5 to 9.3 +/- 0.9 minutes (p = 0.3) after the procedure and wall motion score index at peak dipyridamole changed from 1.55 +/- 0.2 to 1.28 +/- 0.3 (p = 0.05). Forty-nine of 53 grafts were patent as seen on angiography. Dipyridamole echocardiographic results were positive in 4 of 5 patients who had at least 1 obstructed graft or native vessel obstructed distal to bypass graft insertion. The remaining patient had diagnostic electrocardiographic changes during dipyridamole infusion without wall motion abnormalities. Dipyridamole echocardiographic results were negative in all 13 patients who had complete revascularization. In the 4 patients with positive test results, the procedure correctly identified the localization of the diseased bypass graft.(ABSTRACT TRUNCATED AT 250 WORDS)

High dose dipyridamole echocardiography early after uncomplicated acute myocardial infarction: correlation with exercise testing and coronary angiography.

The feasibility, safety and usefulness of dipyridamole echocardiography (two-dimensional echocardiography and 12 lead electrocardiographic monitoring during dipyridamole infusion, up to 0.84 mg/kg over 10 min) were evaluated in 94 asymptomatic patients 8 to 10 days after uncomplicated acute myocardial infarction. The results were compared with those of symptom-limited treadmill exercise testing and correlated with coronary angiography. Two mechanical patterns of positivity of dipyridamole echocardiography could be identified: 1) a new wall motion abnormality confined to the infarct zone or to the adjacent segments (24 patients), and 2) transient remote asynergy (33 patients). The success rate in recording adequate images during dipyridamole infusion was 100%. Interobserver agreement concerning diagnosis occurred in 89 (93%) of 94 patients. Dipyridamole echocardiography was well tolerated; no complication was observed during or after the test. Seventy-three patients underwent coronary angiography within 6 weeks after acute myocardial infarction. Transient remote asynergy on echocardiography was present in 27 of 40 patients with multivessel disease and in none of 33 patients without multivessel disease. Results of treadmill exercise testing were positive in 28 patients with multivessel disease and 8 patients without multivessel disease. Thus, the sensitivity of dipyridamole-induced transient remote asynergy was 68% compared with 52% for treadmill testing (p less than 0.05); specificity was 100% and 72%, respectively (p less than 0.005). The overall accuracy of dipyridamole echocardiography (81%) was higher than that of dipyridamole stress electrocardiography (63%) or exercise electrocardiography (60%) (p less than 0.02). It is concluded that dipyridamole echocardiography is a useful, feasible and inexpensive nonexercise-dependent test for detecting the extent of coronary artery disease early after acute myocardial infarction.

Clinical experience with urokinase in intracoronary thrombolysis.

A prospective nonrandomized study of the thrombolytic efficacy and dose-response effect of a high-molecular-weight urokinase, administered into the coronary artery, was conducted in 63 patients with acute myocardial infarction. Urokinase was infused (up to 180 min) at rates of 2000, 4000, 6000, and 10,000 IU/min in four consecutive groups of patients within 184 +/- 70 min following onset of chest pain. Of 54 patients with complete occlusion of the infarct-related vessel, 48 (89%) exhibited complete reperfusion. In 9 patients with incomplete occlusion, the degree of coronary stenosis was reduced with concomitant improvement in antegrade flow. The median effective dosage requirement of urokinase to reperfuse 50% of the treated patients was 180,000 IU. A relationship between the four infusion regimens and successful reperfusion was not found. The time to reperfusion, however, ranging from 42 +/- 30 to 60 +/- 41 min, appeared to be dose dependent. The reocclusion rate at follow-up (10-14 days) was 18%. Ejection fraction improved (40 +/- 8 vs. 47 +/- 8%, p = 0.002) in patients with low pretreatment values and in those treated within 2 h of the onset of symptoms. In-hospital mortality was 9%. Hemorrhage requiring transfusion occurred in 8% of the patients. None of the patients had levels of circulating fibrinogen inferior to 100 mg/dl. We conclude that urokinase can induce timely coronary reperfusion in patients with evolving myocardial infarction, at moderate infusion rates, and with concomitant induction of an only mild systemic lytic state.

Efficacy of intracoronary and intravenous urokinase in acute myocardial infarction.

The efficacy of intracoronary and intravenous urokinase was studied in 83 patients with acute evolving myocardial infarction. Urokinase was administered intracoronary in 48 patients with a success rate of 89% obtained after 47 +/- 32 minutes of infusion of a dose of 255.000 +/- 224.000 IU. In-hospital mortality in this group of patients was 10%. Severe arrhythmias were observed in 33% of the patients and the reocclusion rate at the re-study was 16%. Intravenous urokinase was administered as 200.000 IU bolus followed by 1.220.000 IU infusion in 21 patients. Angiography performed in this group of patients 48 hours after therapy showed a patency rate of 66%. A single intravenous bolus of 500.000 IU of urokinase was administered to 14 patients. At angiography all patients but one were found reperfused. The value of intravenous low-dose bolus injection of urokinase in acute myocardial infarction needs hower to be assessed with a properly designed clinical trial.

[Intracoronary thrombolysis]. / Trombolisi intracoronarica.

Intracoronary Urokinase administration was attempted in 42 patients with acute myocardial infarction. One patient died before Urokinase infusion could be started, two patients during treatment. 34 patients (83%) had total occlusion of a coronary vessel, 7 patients (17%) had a subtotal occlusion. Urokinase was administered at a rate of 10.000 IU/min in 11 consecutive patients (Group I), 6000 IU/min in 11 patients (Group II), 4000 IU/min in 11 patients (Group III), 2000 IU/min in 8 patients (Group IV). Recanalization of the occluded vessel or amelioration of the subocclusion was obtained in 36 patients (88%). 35 patients were controlled 12 days after the procedure, with coronary-angiography and left ventriculography. Patency persisted in 31 patients and successful thrombolysis was associated with significant improvement of left ventricular ejection fraction in those patients with depressed ventricular function before Urokinase treatment.

[Correlations among the haemodynamic effects in acute myocardial infarction. Function evaluation and prognosis 12 months later (author's transl)]. / Correlazioni tra i valori emodinamici, la fase acuta, l'evoluzione funzionale e la prognosi a 12 mesi nell'infarto miocardico.

The hemodynamic monitoring of acute myocardial infarctions has been carried out in patients less than 75 y.o. who showed: a) extensive anterior myocardial infarction; b) inferior myocardial infarction and ST segment depression of the anterior chest leads; c) acute myocardial infarction and cardiac failure. The hemodynamic measurement were carried out at the 12 hours (mean) from the beginning of chest pain on 65 patients who suffered the first myocardial infarction and were protracted to 60 hours (mean). The hemodynamic findings were classified according to the relationship between the stroke work index of the left ventricle (LVSWI) and the mean pulmonary artery pressure (MPAP) as following: normals: 6 pts; hypovolemia: 15 pts; reduced compliance: 2 pts; mild LV failure: 19 pts; severe LV failure or shock: 23 pts. 35 pts have carried out a complete rehabilitation programme has shown an inverse linear relationship to the MPAP of the first recording in CCU. The incidence of death was 29% one year after the myocardial infarction and showed a significant relationship to the hemodynamic findings. The LVSWI resulted more sensitive than MPAP; 90% of patients who showed a LVSWI less than 20 gmb/m2 died.