Spontaneous coronary artery dissection: a neglected cause of acute myocardial ischaemia and sudden death.

Spontaneous coronary artery dissection is a rare cause of acute myocardial ischaemia. Eight consecutive fatal cases which occurred in women aged 34-54 years (mean 43) are described. The dissection involved the left anterior descending coronary artery in four, the left main trunk in two, the right coronary artery in one, and both left anterior descending and circumflex arteries in one. The clinical presentation was sudden death in six cases, and acute myocardial infarction in two. Diagnosis was made at necropsy in every case but one, in which coronary dissection was diagnosed during life by selective coronary angiography. The only ascertained risk factor was hypertension in one patient; none of the women was in the puerperium, and Marfan syndrome was excluded in all. Histology showed a haematoma between the coronary tunica media and adventitia, that flattened and occluded the lumen; a coronary intimal tear was detected in only two cases. Unusual histological findings were cystic medial necrosis in one case, eosinophilic inflammatory infiltrates in four, and angiomatosis of the tunica adventitia in one. Patients dying of spontaneous coronary dissection are usually middle aged women, with no coronary atherosclerosis and apparently no risk factors. Spontaneous coronary artery dissection is unpredictable, and sudden death is the usual mode of clinical presentation. Prompt diagnosis and life saving treatment is far from being achieved.

[Myocardial infarct with normal coronary vessels: an association with dysfunction of the coronary microcirculation]. / Infarto miocardico con coronarie normali: associazione con la disfunzione del microcircolo coronarico.

The association of acute myocardial infarction (AMI) with normal coronary arteries was analyzed prospectively. A series of 128 consecutive patients underwent coronary angiography within 1 week from AMI. Seven patients, all females, had no coronary artery lesions and were considered eligible for the study. All 7 patients underwent atrial pacing (10 g/min increments every 2 min), ergonovine testing (E; total dose 0.650 mg i.v.). Great cardiac vein flow (GCVF; thermodilution technique), mean aortic pressure (MAP), anterior coronary resistance (ACR) and myocardial lactate extraction [(Lac art-Lac gcv)/Lac art] were measured at baseline and during testing. Pacing-induced typical chest pain occurred in 5 patients: 4 of them showed concurrent significant (> or = 0.15 mV) ST downsloping. At peak pacing, GCVF increased only by < 50%, or even decreased, in all patients. Baseline lactate extraction (0.13 +/- 0.11) changed to lactate production (-0.15 +/- 0.10) in 7/7 patients. None of the patients showed focal epicardial coronary artery spasm following E. During testing, however, all 7 patients showed decrease in GCVF (110 +/- 47 versus 74 +/- 21; p < 0.005), increase in ACR (0.92 +/- 0.29 versus 1.43 +/- 0.20; p < 0.001), and significant coronary lactate production (-0.18 +/- 0.12). Six patients referred slight to moderate chest pain, which was accompanied by ST downsloping in 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in pulmonary hemodynamics predict benefits in exercise capacity after ACE inhibition in patients with mild to moderate congestive heart failure.

Several causes may affect the efficacy of angiotensin-converting enzyme (ACE) inhibitors in congestive heart failure (CHF). The present study was undertaken to identify what factors might predict benefits in exercise capacity after ACE inhibition in 22 patients with mild to moderate CHF. All patients underwent hemodynamic evaluation before and following an oral dose of quinapril (20 mg). They were then treated daily with 20 mg of quinapril and underwent exercise stress test off-drugs 1 day and 6 months later. Patients were grouped according to their relative changes in vascular resistances after quinapril: Group A (n = 15) showed a greater decrease in pulmonary vascular resistance (PVR) than in systemic vascular resistance (SVR) (% delta PVR/% delta SVR > 1). The opposite occurred in Group B (n = 7). Comparison of pretreatment baseline features revealed that the two groups had similar biochemical and hormonal variables, cardiac index, and SVR. Conversely, Group A patients had higher (p < 0.05) pulmonary artery pressure and PVR compared with Group B patients. Following quinapril, Group A patients showed a greater (p < 0.05) increase in cardiac index than Group B patients, despite a similar reduction in SVR. Accordingly, 1-day drug treatment significantly (p < 0.001) increased exercise duration in Group A (+29%), but not in Group B patients (+7%). Benefits in exercise capacity were still significant (p < 0.001) 6 months later.(ABSTRACT TRUNCATED AT 250 WORDS)

Vasotonic angina: a spectrum of ischemic syndromes involving functional abnormalities of the epicardial and microvascular coronary circulation.

OBJECTIVES: The present study was undertaken to investigate the response of large and small coronary arteries in a subgroup of patients with no or minimal coronary artery disease found to have objective signs of myocardial ischemia. BACKGROUND: Many patients apparently have normal coronary arteries despite abnormal electrocardiographic (ECG) changes during spontaneous anginal attacks or exercise stress testing. METHODS: Twenty-five patients with no or minimal (< 30% stenosis) coronary artery disease were chosen from a pool initially selected on the basis of spontaneous anginal attacks and ST segment shifts in the anterior leads. Of these, 10 were grouped as having variant angina (at least one episode of ST elevation) and the remaining 15 as having syndrome X (exercise-induced anginal pain, ST depression and reversible thallium abnormalities). Data were compared with those obtained in 10 patients with stable angina and documented coronary artery disease. Eighteen patients with supraventricular arrhythmias and normal coronary arteries served as control patients. Patients showing focal spasm during ergonovine testing were not included in the subsequent angiographic analysis. Great cardiac vein blood flow, aortic pressure and changes in coronary artery diameter were measured at rest and 2 to 4 min after hyperventilation in the remaining study group. The same procedure was repeated after sublingual administration of 0.3 mg of nitroglycerin in eight patients (four with syndrome X and four with variant angina). RESULTS: Hyperventilation induced diffuse epicardial coronary diameter reduction, which was marginal in control patients (9 +/- 4%) and those with coronary artery disease (5 +/- 3%) but severe (p < 0.001) in those with variant angina (28 +/- 14%) or syndrome X (25 +/- 13%). Concomitant determination of coronary blood flow showed significant (p < 0.001) decreases in those with variant angina (25 +/- 11%) and syndrome X (28 +/- 10%) but not in control patients (5 +/- 8%) or those with coronary artery disease (4 +/- 5%). Changes in great cardiac vein blood flow during hyperventilation were similar before and after nitroglycerin. CONCLUSIONS: These findings indicate that vasoconstrictor stimuli may trigger a diffuse abnormal response of both epicardial and resistance vessels in some patients with chest pain and angiographically normal coronary arteries. Patients showing such diffuse vasoconstrictor abnormalities are suggested to have a single pathogenetic entity with a spectrum of ECG manifestations ranging from ST depression to ST elevation.

[Regional coronary blood flow in patients with acute myocardial infarct treated by systemic fibrinolysis]. / Valutazione del flusso coronarico regionale in pazienti con infarto miocardico acuto trattati con fibrinolisi sistemica.

Thrombolysis has been reported to restore coronary blood flow in patients with acute myocardial infarction (AMI). However, the relationship between fibrinolytic treatment and evidence of myocardial reperfusion has not been adequately assessed. Accordingly, we measured great cardiac vein blood flow (GCVF:thermodilution) in 12 patients (Group 1) presenting with AMI (chest pain < 4 hours and ST elevation in the anterior leads) before and following i.v. urokinase (UK:2 million U/90 min). Ten patients receiving conventional treatment served as controls (Group 2). UK induced a significant increase of GCVF (from 101 +/- 24 to 164 +/- 42 ml/min, p < 0.001). Maximal increase occurred after 50 +/- 54 min from drug infusion. Conversely, changes in GCVF were not significant in Group 2 (from 103 +/- 35 to 106 +/- 31 ml/min, NS). Following 24 hours changes in GCVF were still consistent only in Group 1 patients. Individual analysis during 24 hours showed marked fluctuations of GCVF peak values in Group 1 patients (62 +/- 43%), but not in Group 2 (29 +/- 21%). Thus, UK induces a marked increase of GCVF in most patients with anterior AMI; such increase suggests that reperfusion occurs early (i.e. within 1 hour) from UK administration. Fluctuations of GCVF during monitoring are magnified by thrombolysis, suggesting intermittent coronary reocclusion in the early hours of AMI.

[The differentiated effects of fibrinolysis on the coronary flow in patients with unstable angina]. / Effetti differenziati della fibrinolisi sul flusso coronarico in pazienti con angina instabile.

BACKGROUND: Intracoronary (i.c.) thrombus is a frequent finding in patients (pts) with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. METHODS: To test this hypothesis we studied 13 pts with UA refractory to maximal medical treatment and ST segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all pts within 48 hours (mean 29 +/- 13 hrs) from the last chest pain episode. Following angiography, pts received i.v. wrokinase (UK: 1 million IU/30 min); aortic pressure and GCVF were measured before and every 10 min during drug infusion, for a total time of 90 min. RESULTS: At baseline angiography 5/13 pts (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 pts (Group 2) did not. Overall, coronary hemodynamics did not change significantly following drug administration: GCVF was 103 +/- 65 on baseline and 117 +/- 68 ml. min after UK; p > 0.05. Conversely, group analysis showed that UK increased GCVF and decreased anterior coronary resistances (mean aortic pressure/GCVF) in Group 1 (respectively from 86 +/- 33 to 114 +/- 41 ml. min: p < 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml. min: p < 0.05) but not in Group 2 (both: p > 0.05), despite similar effects on aortic pressure. CONCLUSIONS: Fibrinolytic treatment can be of therapeutic value in UA; UK has shown to increase regional coronary blood flow in selected pts presenting with refractory angina as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Coronary hemodynamic effects of systemic thrombolysis in patients with unstable angina.

Intracoronary (i.c.) thrombus is a frequent finding in patients with unstable angina (UA). Accordingly, thrombolytic treatment could be beneficial, as resolution of thrombus might result in increased delivery of blood flow to the ischemic regions. To test this hypothesis, we studied 13 patients with active UA and ST-segment shift in the anterior leads. Coronary angiography was performed and great cardiac vein blood flow (GCVF; thermodilution) was measured in all patients 25 +/- 14 h after the last chest pain episode. Following angiography, patients received i.v. urokinase (UK: 1,000,000 IU/30 min); aortic pressure and GCVF were measured before and every 10 min following drug infusion, for a total time of 90 min. At baseline angiography, 5 of 13 patients (Group 1) had evidence of i.c. thrombus (intraluminal filling defect or thrombotic subocclusion) in the ischemia-related left coronary artery, whereas 8 patients (Group 2) did not. Group analysis showed that UK increased GCVF and decreased anterior coronary resistance in Group 1 (respectively, from 86 +/- 33 to 114 +/- 41 ml/min: p less than 0.005; and from 1.37 +/- 0.68 to 1.01 +/- 0.44 mmHg/ml/min: p less than 0.05) but not in Group 2 (both: p = NS). In conclusion, UK has been shown to increase regional coronary blood flow in selected patients presenting with active UA, as well as evidence of i.c. thrombus at early angiography. Heterogeneity of angiographic findings could explain controversies in trials dealing with thrombolysis in UA.

Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome.

Complex stenosis morphology frequently occurs in patients with unstable angina pectoris. However, its relation to transient myocardial ischemia and hospital outcome has not been ascertained. To address this issue, 88 patients with significant (greater than or equal to 50%) coronary artery disease presenting with angina--new onset (n = 38), worsening (n = 20) or at rest (n = 30)-were studied. Patients with left main artery disease, normal coronary arteries or occlusion of the ischemia-related arteries were not included in the study. Continuous electrocardiographic recordings were obtained during the first 24 hours. Angiography was performed within 1 week from admission. Complex morphology was defined as any stenosis with irregular borders, overhanging edges or intracoronary thrombus. Only data referring to the in-hospital outcome were considered in this study. Adverse end points were sudden death, myocardial infarction and emergency revascularization. Analysis of the angiograms revealed a complex morphology in 58 patients (group 1). The remaining 30 patients served as control subjects (group 2). Thirty-two of the 58 group 1 patients had an unfavorable clinical outcome (positive predictive value, 55%). A similar outcome occurred in only 2 of the 30 group 2 patients (negative predictive value, 93%). Of the 32 group 1 patients who had an unfavorable clinical outcome, 29 had a cumulative duration of transient myocardial ischemia of greater than or equal to 60 minutes per 24 hours. A similar duration of ischemia, however, was observed in another 6 group 1 and in 8 group 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

[Variant angina which interacts with two phenomena: local hypersensitivity and abnormal response in the coronary tree to vasoconstrictor stimuli]. / L'angina variante quale interazione tra 2 fenomeni: ipersensibilità locale ed abnorme risposta dell'albero coronarico agli stimoli vasocostrittori.

The aim of the present study was to evaluate the vasomotion of the entire coronary tree in variant angina, particularly focusing the attention on the behaviour of the "non spastic" epicardial vessels, using a quantitative coronary technique. Two different groups of patients served as controls. The first group consisted of 10 patients with accessory nodal pathway but without any sign of myocardial ischemia (Group I). The second group included 8 patients with stable exertional angina pectoris and coronary artery disease (Group II). The third group (Group III) consisted of 16 patients presenting with variant angina and spontaneous or hyperventilation-induced (HV: 30 cycles/min for 5 min) ST segment elevation. All patients underwent coronary angiography before and 2 min after HV testing; the evaluation of the coronary diameters was performed on baseline and after HV. In Group III, the HV testing caused a 26 +/- 12% reduction of the "non spastic" coronary vessels, with the mean control diameter of 2.00 +/- 0.61 mm that decreased to 1.48 +/- 0.55 mm. The patients of Group I showed only a mild degree of vasoconstriction (9 +/- 6%) of the epicardial coronary vessels; the Group II patients, also, showed a moderate response to vasoactive stimulus (11 +/- 8%), with the mean control diameter of 2.36 +/- 0.69 mm that decreased to 2.09 +/- 0.65 mm. The greater amount of vasoconstriction showed by patients with variant angina was statistically significant compared to both control groups (p less than 0.001). A further analysis of the coronary vasomotion, in Group III patients, showed that the 6 patients with normal or near normal coronary angiograms exhibited a 34% reduction in the vessel diameter. The remaining 10 patients who presented with a diffuse atherosclerotic involvement of the epicardial vessels (organic stenosis greater than or equal to 50% at the site of spasm) showed a lesser (20%) but yet significant extent of vasoconstriction compared to both control groups (p less than 0.001). In conclusion, our data indicate that: patients with variant angina exhibit a marked and diffuse coronary narrowing of the coronary vessels during vasoconstrictor stimuli; focal spasm occurs more frequently at the level of atherosclerotic coronary segments, whether they are critical or not. An interaction between these 2 phenomena, ie atherosclerosis and abnormal vasoconstriction, is supposed to be a cause of the occurrence of focal coronary spasm in variant angina.

[Abnormal coronary response to vasomotor stimuli: analogies between variant angina and X syndrome]. / Abnorme risposta coronarica a stimoli vasomotori: analogie tra angina variante e sindrome X.

The aim of this study was to evaluate the effects of hyperventilation (HV) and of ic nitroglycerin (NTG) on coronary diameters and hemodynamics in 32 patients with angina pectoris. Of these, 10 patients had stable angina and critical coronary artery disease (CAD, Group I), 12 patients with variant angina (VA) and no or minor coronary atherosclerosis (Group II), and 10 patients with angina and normal coronary arteries (syndrome X (SX), Group III). All patients underwent coronary angiography as well as right heart catheterization; measurements of left anterior descending coronary diameters (mid segment), great cardiac vein blood flow, aortic pressure and coronary resistance were performed on baseline, after HV and following NTG. HV caused coronary spasm in 4 patients with VA and significantly (p less than 0.001) reduced coronary diameters and regional blood flow both in Groups II and III, but not in Group I. NTG resulted in increased coronary diameters in all patients, however variations were greater in VA and SX (44 and 39%, respectively) than in Group I (18%; p less than 0.025). NTG induced an increase of coronary blood flow only in patients with CAD. We conclude that patients with VA and SX present a similar coronary response to vasomotor stimuli, either after HV or following NTG. Response is abnormal if compared to that of patients of group I, and it involves both epicardial and intramural coronary vessels. Thus, we suggest that SX and VA belong to a single pathogenetic entity with a spectrum of clinical manifestations.

Echo-phonocardiographic evaluation of the Björk-Shiley mitral prosthesis.

Ninety patients were studied with combined echophonocardiography after Björk-Shiley disc prosthetic mitral valve replacement. They were evaluated every 6 months (mean follow-up 6 years). Nine cases of left ventricular (LV) failure and 6 cases of prosthetic malfunction (5 paravalvular leaks and 1 thrombosis) were detected; 1 case was confirmed at necropsy and the other 5 cases were surgically verified and repaired. The following measures of prosthetic malfunction were evaluated: opening and closing velocity, maximal amplitude of the prosthesis, septal motion 6 months after operation, LV diastolic diameter, protodiastolic hump, variations during same record of the interval between aortic valve closure sound to the phono and mitral valve opening to the echo, and interval between aortic valve closure sound and maximal excursion of the LV posterior wall. All measures studied were useful for detecting prosthetic malfunction, but 2 are more useful in individual cases: variations of the interval between second heart sound and mitral valve opening and the interval between the aortic valve closure sound and LV posterior wall motion. These 2 intervals also allow discrimination between normal function, prosthetic malfunction and LV failure.

[Value of metabolic studies in diagnosis of ischemic cardiopathy]. / Valore dello studio metabolico nella diagnostica della cardiopatia ischemica.

10 patients with documented heart disease were undergone to atrial pacing (AP) combined to metabolic study. A negative lactate utilization (-%L) noticed in SC (coronary synus) represents a sure proof of a subordinate pacing ischaemia. As the negative lactate utilization is absent a significative reduction of %L during AP or its persistence in recovery and a rise of L/P are further parameters of a subordinate pacing ischaemia. The Authors consider the usefulness of combining a metabolic study to AP in assessing the RC (coronary reserve).