Cases in electrocardiography.
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Biomedical subjects
Publications and source records attributed to C Vassanelli.
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In the assessment of the acute results of percutaneous transluminal coronary angioplasty (PTCA), myocardial perfusion at maximal vasodilatation theoretically has fewer limitations than the coronary flow reserve measurements and quantitative coronary angiography. The purpose of this study was to compare the myocardial perfusion to the measurements of the severity of the lesion (minimal luminal diameter and percent area stenosis) and to relate it to the changes of left ventricular function after PTCA. Regional myocardial perfusion was assessed during intracoronary papaverine, using the inverse mean transit time of contrast medium (1/Tmn), before, 15 min after, 18-24 hr after, and 6 months after successful single-vessel PTCA in 14 patients with stable angina. Left ventricular angiography (before angioplasty, 18-24 hr after, and 6 months later) was analysed by area-length and centerline methods. Immediately after PTCA, 1/Tmn increased from 0.14 +/- 0.07 sec-1 to 0.21 +/- 0.09 sec-1 (P = .001). Maximal myocardial perfusion remained higher than the pre-PTCA value the day after angioplasty (1/Tmn of 0.23 +/- 0.09 sec-1), while it reduced to near pre-PTCA values at follow-up (1/Tmn of 0.16 +/- 0.05 sec-1). Before PTCA, three out of ten patients had ejection fraction of < 65%, and seven had mild-to-moderate hypokinesis. The day after PTCA the ejection fraction and the regional dysfunction improved significantly. The change in ejection fraction 18-24 hr after PTCA did not correlate with minimal luminal diameter and percent area stenosis and correlated slightly with the improvement of perfusion (r = 0.54, P = .10). At follow-up left ventricular function deteriorated in the whole group, despite the persistence of angiographic success of PTCA, possibly because of changes in the loading condition. Coronary artery stenosis measurements and 1/Tmn failed to correlate with the left ventricular function. Given the difficulties in routine application of the analysis of time-density curves, the measurement of minimal luminal diameter remains a more practical assessment of the results of the intervention. However, the improvement of myocardial perfusion may give more information than coronary artery dimensions of the early recovery of left ventricular function.
Short-term outcome after coronary angioplasty is mainly determined by restenosis, while long-term outcome is determined by new events due to incomplete revascularization, by atherosclerosis progression and by late-restenosis. The aim of this study is to assess if correctly treated coronary risk factors are predictors of poor prognosis after coronary angioplasty. Two-hundred and twenty six patients (209 males, 17 females, mean age 56 +/- 9 years) with successful coronary angioplasty were treated for coronary risk factors. New events (death, myocardial infarction, repeat angioplasty, bypass surgery) were recorded. Ischemia was evaluated by serial exercise tests. The mean follow-up was 31 +/- 12 months. Survival was 99.5% at 1 year and 97.4% after 5 years; "event free survival" was 84.6% at 1 year and 65.9% after 5 years; "ischemia free survival" was 84.6% at 1 year and 44.8% after 5 years. "Ischemia free survival" was higher in patients with single coronary angioplasty and in patients with infarct-related vessel angioplasty. Smoke addiction, diabetes, hypercholesterolemia and hypertension were not significantly correlated with "ischemia free survival". Smokers and diabetics had a trend towards a less favorable 5 year outcome, but without statistical differences. In conclusion, this study shows that correctly treated coronary risk factors do not worsen prognosis after coronary angioplasty.
BACKGROUND: Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction). METHODS: Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment. RESULTS: In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not. CONCLUSIONS: Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.
BACKGROUND: When used in the setting of acute myocardial infarction, intravenous thrombolytic agents fail to achieve early infarct artery patency in 15% to 50% of patients. We tested the hypothesis that immediate balloon angioplasty applied to patients with failed early reperfusion would improve left ventricular function and clinical outcome at 30 days compared with conservative management alone. METHODS AND RESULTS: One hundred fifty-one patients with first anterior wall infarction treated with any accepted intravenous thrombolytic regimen and angiographically demonstrated to have an occluded infarct vessel within 8 hours of chest pain onset were randomized to aspirin, heparin, and coronary vasodilators (conservative therapy) or to this therapy and balloon angioplasty supplemented by further thrombolytic therapy as needed. Left ventricular function was assessed using multiple-gated equilibrium radionuclide technique to determine ejection fraction, and adverse clinical outcome was assessed evaluating death, ventricular tachycardia, and class III or IV heart failure at 30 days. Seventy-three patients were randomized to conservative therapy and 78 to angioplasty. The two groups were well balanced for patient age (59 +/- 11 years), sex (82% were male), and time to randomization (4.5 +/- 1.9 hours). Angioplasty was technically successful in 72 of 78 randomized patients (92%). Two patients randomized to conservative therapy crossed over to angioplasty within 72 hours. Resting 30-day ejection fraction was 40 +/- 11% in the angioplasty group and 39 +/- 12% in the conservative group (P = .49), but ejection fraction with exercise was 43 +/- 15% and 38 +/- 13% for the angioplasty and conservatively treated groups, respectively (P = .04). Adverse clinical outcomes included death in 5% and 10% (P = .18), severe heart failure in 1% and 7% (P = .11), and either death or severe heart failure in 6% and 17% (P = .05) of the angioplasty and conservatively managed groups, respectively. CONCLUSIONS: When applied to patients with first anterior infarction, rescue angioplasty appears to be useful in the prevention of death or severe heart failure, with improvement in exercise, but not resting, ejection fraction. This strategy deserves further study and highlights the potential advantage of early mechanical restoration of infarct vessel patency when thrombolytic therapy has failed.
Coronary stenting is a technique complementary to coronary angioplasty, because it is successful in the management of the two major limitations of conventional balloon dilation, i.e. the acute or threatened closure and the restenosis. The currently available intracoronary stents are far from being ideal, mainly for their thrombogenicity. During abrupt closure, the bailout stenting has, in most of the cases, offered a valuable alternative to emergency coronary artery bypass surgery. The major complications after stent insertion are the result of an inadequate stent placement, of persistence of intra and/or poststent obstruction and of the ineffective anticoagulant therapy. The mechanical support (scaffolding) provided by the stent after dilation significantly reduces the amount of elastic recoil, and, improving laminar flow, eliminates arterial wall shear stress that may contribute to an increase in intimal thickening. Moreover, the reduction of arterial cyclical stretching may reduce the rate of neointimal proliferation. By sealing the exposed subintimal spaces, stents may minimise the formation of local thrombi, and thus also limit their later organization and fibrous conversion into part of the restenotic lesion: two recently completed randomized trials (STRESS and BENESTENT) confirm the lower rate of restenosis in patients treated with single stent placement in de-novo lesions as compared with standard balloon angioplasty. The mechanism of stent benefit in reducing restenosis rate seems to be the wider initial lumen, which can accommodate a greater degree of intimal hyperplasia. In the near future, the improvements of the blood and tissue compatibility of the stents, may allow easier management.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute myocardial infarction is a rare complication of ascending aortic dissection; it is usually due to the coronary ostium involvement. The authors describe an unusual case with anomalous left coronary origin too; they suggest that, due to this combination, the aneurysmatic area pushes the anomalous coronary artery, causing acute myocardial infarction.
Several studies have shown evidence of the key role of the endothelium in modulating the tone of epicardial coronary vessels, in the different manifestations of coronary artery disease. Recently, the role of endothelium-dependent vasodilation has been focused, because clinical observations have suggested that myocardial ischemia might be caused or aggravated by inappropriate vasoconstriction of resistance vessels. An abnormal endothelium-dependent vasodilation, either of epicardial and of coronary microvasculature, has been documented in patients with syndrome X and in patients with history of hypertension and left ventricular hypertrophy. Vasoconstriction of the small coronary vessels is probably the mechanism underlying the impaired increase of coronary blood flow during atrial pacing and the wide variations of the ischemic threshold in some patients with chronic stable angina. In patients with variant angina, the endothelial function seems abnormal only in the conductance vessels. It is likely that the endothelial dysfunction of the small coronary arteries be present in many clinical situations in which a discrepancy between a mild atherosclerosis of epicardial coronary artery and signs of ischemia exists, as it has been observed early after successful angioplasty and after coronary artery reperfusion during acute myocardial infarction.
It is generally accepted that Lp(a) is an independent risk factor of cardiovascular diseases. Since the apolipoprotein component of Lp(a) shows some homologies to plasminogen, it is, however, unclear as to whether the pathological effect is due to the role played by the lipoprotein in lipid metabolism or in the fibrinolytic system. We compared two groups of patients with myocardial infarction, with and without angiographically documented coronary artery disease. In the latter group, imbalances in the clotting system are very likely, while members of the former group may also display disturbances of lipid metabolism. The results show that the two groups display differences in lipid metabolism, whereas they have similar patterns of thrombogenicity indices and Lp(a) values. This study seems to support the hypothesis that Lp(a) does play a role in the fibrinolytic system, since even those myocardial infarctions without obstructive coronary artery disease have a high frequency of Lp(a) concentrations above 300 mg/l, i.e. similar to the situation found in the myocardial infarctions with angiographically documented coronary artery disease. Whether the high Lp(a) concentrations in the two groups are related to an impaired fibrinolysis will be the subject of further investigation.
In 24 patients 2 leads Holter monitoring was performed during percutaneous transluminal coronary angioplasty (PTCA) of left anterior descending (17 patients), right coronary artery (6 patients), left circumflex (1 patient). In 20 patients (83%) significant ST segment deviations were recorded in the lead CM2 or RV. The following characteristics of ST segment deviation were analyzed during 7 +/- 3 successive occlusions: time to onset, maximal ST shift, slope to development, time to onset and slope of ST segment normalization. In 17 patients with successful PTCA the slope of ST segment normalization increased progressively from the first to the third-fifth inflation and then was constant. The improvement in ST segment normalization velocity was correlated (p less than 0.01) with the reduction of the diameter and with improvement of sectional area of the dilated vessel. The maximal ST segment normalization slope was correlated (p less than 0.01) with the diameter and the area of the residual stenosis. Continuous electrocardiographic recording, during PTCA, for evaluation of ST segment normalization velocity is a promising approach for monitoring the immediate result of coronary angioplasty.
Intravascular ultrasound angioscopy allows to better define the structure of arterial wall and the effect of angioplasty. We report the case of a patient previously treated by coronary angioplasty, who underwent peripheral angioplasty for a stenosis of the left iliac artery. Intravascular ultrasound imaging performed before and after balloon dilatation clearly identified the plain of dissection and the partial resolution of the stenosis in a better way compared to digital angiography.
Myocardial ischemia with normal coronary arteries can be due to anatomic or functional reasons. The more severe congenital coronary anomalies in the adulthood are the origin of the left main of the left coronary artery from the right aortic sinus, with a course between the aorta and the pulmonary trunk, and the origin of the left main from the pulmonary trunk. Both these anomalies can cause sudden death, usually associated with physical exertion. The coronary vasomotion of epicardial vessels depends on the interaction of several neurohumoral substances. We report the hemodynamic, angiographic and stress test data of 30 patients affected by chest pain, with myocardial ischemia and normal coronary arteries. In 8 patients the response of epicardial coronary arteries to intracoronary infusion of acetylcholine was evaluated.
Myocardial infarction and normal coronary arteries is not a rare event in the ischemic heart disease. Even if the patients with acute myocardial infarction and angiographically normal coronary arteries represent a small percentage (reported incidence varies from 1% to 12%) of all patients with acute ischemic attacks, they might be useful to highlight the pathogenetic mechanisms of this syndrome. To improve the understanding of this clinical entity, we reviewed our experience of 18 patients with myocardial infarction and normal coronary arteries. They were compared with a control group of patients with similar clinical characteristics (gender, age, infarct location) and residual coronary artery stenosis. The myocardial damage was less extensive in patients without residual stenosis (peak CK-MB: 56.1 +/- 71.9 vs 126.5 +/- 87.9 IU/I, p < 0.05), with a better left ventricular function either global (ejection fraction: 64 +/- 11 vs 55 +/- 13%, p < 0.05) and regional (SD/chord: -1.36 +/- 1.20 vs -2.42 +/- 1.04, p < 0.02). These findings probably reflect a more prompt and complete reperfusion of the infarct related artery. Myocardial necrosis may occur without obstructive coronary artery disease by the interaction of multiple factors such as abnormal platelet aggregation, thrombus formation and localized or diffuse changes of coronary vascular tone.
With the aim of investigating the functional result of the coronary angioplasty (PTCA) and verifying the predictive value of the exercise test for detecting restenosis, 165 patients who underwent successful PTCA were evaluated through exercise stress tests performed 10, 75 and 165 days after PTCA and through coronary angiography performed 5 to 6 months after PTCA. The percentage of negative tests and the rate-pressure product (RPP) increased significantly with respect to the tests performed before PTCA, both in patients with single-vessel and those with multivessel disease. Maximal ST segment depression and ST/HR were significantly reduced only in patients with complete revascularization. The percentage of positive tests 10 days after PTCA was lower in patients with single-vessel than in those with multivessel disease (2.5% versus 10.8%) and, of the latter, in patients with complete rather than incomplete revascularization (0% versus 13.5%). In patients with complete revascularization, the mean exercise time rose significantly (703 s versus 538 s). The percentage of positive tests increased progressively with time, in accordance with probable increasing restenosis. In comparison with the results of angiography, sensitivity of the exercise stress test proved to be poor (59%), especially in patients with single-vessel disease (45%), while the specificity was very high (98%). The predictive value of a negative test was 77% in patients with multi-vessel and 87% in patients with single-vessel disease. The predictive value of a positive test was over 90% in both groups of patients.
A patient with chronic exertional angina and electrocardiographic signs of myocardial ischemia at exercise stress test had recent onset of rest chest pain and underwent coronary arteriography. Besides severe atherosclerotic coronary disease (which was probably responsible for clinical presentation), a single coronary artery arising from the left sinus of Valsalva was discovered. This is an exceptional finding, and its in-life diagnosis may be relevant for surgical treatment.
Chronic total coronary occlusion is a growing indication to percutaneous transluminal coronary angioplasty. Since primary success of balloon angioplasty in this condition is usually limited by the difficulty of crossing the occlusion, different techniques have been described for this purpose, such as use of stiff guidewires, coronary infusion catheters, guidewires with an olive-shaped tip, or new developing methods (atherectomy, laser), in association with balloon dilatation. Here, we describe our initial experience with a thick (0.035 in) and relatively stiff open-ended guidewire, which has an inner (0.018 in diameter) lumen provided with a core wire. Several advantages are considered. The core wire yields a perfect means of steerability of the whole system, while pushability of a thicker guidewire is much greater. Moreover, the core wire can be removed, and contrast injections beyond the occlusion through the inner lumen can assure proper intraluminal location. Finally, position across the occlusion can be kept easily, since an exchange wire for conventional balloon catheters can be inserted in the inner lumen of the open-ended guidewire.
Five coronary arterial aneurysms were found in 4 of 80 (5%) patients who underwent elective coronary arteriography 6 months after successful percutaneous transluminal coronary angioplasty. None of them was present immediately after dilatation. All patients had been suffering from stable angina before angioplasty, while no case had recurrent angina or definite angiographic restenosis at the 6-month follow-up. Quantitative coronary angiography was performed in all angiograms. The coronary aneurysms only developed in the dilated portions (4 in left anterior descending and 1 in an intermediate branch of the left coronary artery): their diameter ranged from 3.1 to 4.4 mm, and their length from 2.2 to 4.9 mm. The ratio between the aneurysm diameter and the coronary arterial diameter (aneurysm: artery ratio) varied from 1.15 to 1.91 (mean 1.47). No significant clinical or technical differences were found between patients who developed aneurysm after angioplasty, and patients who did not. On the other hand, 4 of the 5 patients who developed aneurysm had angiographic evidence of "non-pathologic" dissection immediately after balloon dilatation. Moreover, the ratio between the measured angiographic diameters of the balloon (at maximal inflating pressure) and of the coronary artery selected for the procedure showed that the balloon was mildly oversized (balloon: artery ratio ranging from 1.10 to 1.37, mean 1.28) in all cases with aneurysm except the only 1 in whom dissection did not occur. In conclusion, aneurysm formation after coronary angioplasty is not infrequent in our experience: balloon size and wall dissection seem to be the major factors related to this event.
In 35 patients with effort angina exercise tests before and after coronary angioplasty (PTCA) were compared, aimed at evaluating functional improvement and at correlating some ergometric parameters with angiographic results. All tests were performed during therapy with verapamil 360 mg/die. After PTCA mean diameter of the stenosis was reduced from 68 +/- 11% to 19 +/- 12%. Duration of exercise and rate-pressure product (RPP) were significantly greater in the test after PTCA. While all tests before PTCA were positive, after PTCA ST segment depression occurred in 9 patients (26%). In 7 of these patients it was less than 1 mm. In 26 patients (74%) tests were negative after PTCA. In patients with ST segment depression, ischemia threshold significantly rose from 5.2 +/- 1.5 min (RPP 15,875 +/- 3,253 to 7.6 +/- 1.2 min (RPP 20,157 +/- 3143). Maximal ST segment depression and ST/HR slope were significantly reduced. In negative stress tests the time free from ischemia significantly rose from 6.5 +/- 2.6 min (RPP 18,872 +/- 3,861) to 10.5 +/- 2.3 min (RPP 28,476 +/- 4,289). In patients with positive tests stenosis after PTCA was more severe than in patients without ST segment depression (29 +/- 13% vs 17 +/- 13%). In patients with ST segment depression improvement of ischemia threshold and of stenosis were correlated. In these patients improvement of ischemia threshold is the ergometric parameter more useful to evaluate the angiographic result of PTCA.