Cardiothoracic ratio may be misleading in the assessment of right- and left-ventricular size in patients with repaired tetralogy of Fallot.

AIM: To assess the relationship between cardiothoracic ratio (CTR) and ventricular and atrial volumes in patients with repaired tetralogy of Fallot (TOF). MATERIALS AND METHODS: Patients with repaired TOF undergoing cardiac magnetic resonance (CMR) and chest radiography within 1 day were included (n = 82; median age: 24.7 years, interquartile range: 21.5-35.9). The CTR was obtained from upright posteroanterior chest roentgenograms. Analyses of CMR images and radiographs were performed in a blinded fashion. RESULTS: There were 35.1% (13/37) of patients with normal CTR (<0.5) who had severe right ventricular (RV) dilatation. There were six patients (13.3%, 6/45) with high CTR with both normal RV and left-ventricular (LV) volumes. CTR did not correlate with either RV or LV volumes but showed a weak correlation with right- and left-atrial volumes (r = 0.43, p = 0.0001; r = 0.27, p = 0.01, respectively). CTR ≥0.5 showed poor ability in the identification of severe RV dilatation (sensitivity: 61.8%, specificity: 50%). The combination of CTR and signs of RV enlargement on lateral radiographs did not improve the diagnostic accuracy of any of those parameters alone. CONCLUSION: CTR in patients with repaired TOF reflected atrial rather than ventricular dilatation. The use of CTR or lateral radiographs in patients with repaired TOF may lead to false conclusions concerning ventricular size.

Stable right ventricular size and function during short-term follow-up in patients with pulmonary regurgitation after tetralogy of Fallot repair.

AIM: To assess changes in ventricular size and function over time in conservatively treated adult patients with repaired tetralogy of Fallot (TOF) and significant pulmonary regurgitation (PR). MATERIALS AND METHODS: Patients with repaired TOF who had undergone more than one cardiac magnetic resonance study were identified. To confine the cause of ventricular size and function deviation to PR, patients with residual ventricular septal defect, more than mild regurgitation at a valve other than the pulmonary valve, and known coronary artery disease were excluded. RESULTS: The final analysis included 27 adults with PR fraction >20%. During a follow-up of mean 2.1 ± 0.8 years, there was no change in right ventricular (RV) end-diastolic volume (EDV; 162.1 ± 27.6 versus 164 ± 29.6 ml/m(2), p = 0.5). Left ventricular (LV) EDV showed a small decrease (85.1 ± 16.2 versus 81.5 ± 14.1 ml/m(2), p = 0.02). The mean PR fraction, PR volume, and peak RV outflow tract gradient did not change. Additionally, both RV ejection fraction (EF) and LVEF remained stable over the follow-up period (48.1 ± 6.5 versus 48.4 ± 6.7%, p = 0.83, and 57.3 ± 5.4 versus 57.2 ± 5.1 %, p = 0.91, respectively). Only two asymptomatic patients (7.4% of the study group) developed symptoms and the remaining did not deteriorate. CONCLUSION: The RVEDV, RVEF, and LVEF remained stable over a mean follow-up of approximately 2 years in the majority of adult patients after TOF repair with significant PR and a wide range of RVEDV.

In vivo and in vitro examination of the functional significances of novel lamin gene mutations in heart failure patients.

CONTEXT: Lamin A/C (LMNA) gene variations have been reported in more than one third of genotyped families with dilated cardiomyopathy (DCM). However, the relationship between LMNA mutation and the development of DCM is poorly understood. METHODS AND RESULTS: We found that end stage DCM patients carrying LMNA mutations displayed either dramatic ultrastructural changes of the cardiomyocyte nucleus (D192G) or nonspecific changes (R541S). Overexpression of the D192G lamin C dramatically increased the size of intranuclear speckles and reduced their number. This phenotype was only partially reversed by coexpression of the D192G and wild type lamin C. Moreover, the D192G mutation precludes insertion of lamin C into the nuclear envelope when co-transfected with the D192G lamin A. By contrast, the R541S phenotype was entirely reversed by coexpression of the R541S and wild type lamin C. As lamin speckle size is known to be correlated with regulation of transcription, we assessed the SUMO1 distribution pattern in the presence of mutated lamin C and showed that D192G lamin C expression totally disrupts the SUMO1 pattern. CONCLUSION: Our in vivo and in vitro results question the relationship of causality between LMNA mutations and the development of heart failure in some DCM patients and therefore, the reliability of genetic counselling. However, LMNA mutations producing speckles result not only in nuclear envelope structural damage, but may also lead to the dysregulation of cellular functions controlled by sumoylation, such as transcription, chromosome organisation, and nuclear trafficking.

Clinical and therapeutic profile of patients presenting with acute coronary syndromes who do not have significant coronary artery disease.The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) Trial Investigators.

BACKGROUND: A proportion of patients who present with suspected acute coronary syndrome (ACS) are found to have insignificant coronary artery disease (CAD) during coronary angiography, but these patients have not been well characterized. METHODS AND RESULTS: Of the 5767 patients with non-ST-segment elevation ACS who were enrolled in the Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin (Eptifibatide) Therapy (PURSUIT) trial and who underwent in-hospital angiography, 88% had significant CAD (any stenosis >50%), 6% had mild CAD (any stenosis >0% to

Myocardial perfusion and function of the systemic right ventricle in patients after atrial switch procedure for complete transposition: long-term follow-up.

OBJECTIVES: Our purpose was to assess the right ventricular (RV) function and identify patients with RV impairment long after the Mustard or Senning operation. BACKGROUND: Systemic ventricular failure can cause myocardial perfusion abnormalities in thallium scintigraphy correlating with hemodynamic deterioration. METHODS: Myocardial perfusion at rest and at peak exercise was assessed in 61 patients, aged 7 to 23 years in mean time 10.0 +/- 2.9 years after surgery using technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography. Ventricular function was assessed by first-pass radionuclide angiography at rest. Exercise capacity was determined with a modified Bruce protocol. RESULTS: The mean RV ejection fraction was 36.1 +/- 7.7%, and left ventricular (LV) ejection fraction was 52.1 +/- 9.4%. Moderate or severe perfusion abnormalities on the rest scan were observed in 20 patients (33%). On exercise perfusion worsened in another 13 patients (21.3%). Patients with perfusion defects on stress scan had significantly lower RV and LV ejection fraction (33.2 vs. 39.4%; p = 0.002 and 49.2 vs. 55.5%; p = 0.01, respectively). They were also older (16.6 vs. 13.0 years; p = 0.002), operated on at an older age (4.0 vs. 2.4 years; p = 0.05) and had longer follow-up (12.5 vs. 10.5 years; p = 0.003). CONCLUSIONS: Myocardial perfusion defects are common findings in patients in long-term follow-up after atrial switch operation. Despite excellent exercise tolerance, the extent of myocardial perfusion abnormalities correlated well with impaired RV and LV function, and greater perfusion defects were seen more frequently in older patients with longer follow-up. It is likely that myocardial perfusion defects could be a sensitive predictor of systemic ventricular impairment.

Apparent inosine uptake by the human heart.

Although inosine has been used clinically to support the myocardium, no data are available on the fate of exogenous inosine in the human heart. We therefore infused six patients, catheterised for coronary angiography, with inosine (5 mg.kg-1.min-1 intravenously) for 6 minutes. Before infusion, the arterio-venous difference of inosine, hypoxanthine and xanthine across the heart was nil. During infusion, arterial inosine increased substantially, exceeding the coronary sinus concentration by a maximum of 200 (SEM 53) mumol.litre-1, p = 0.02, at the fourth minute. Arterial hypoxanthine and xanthine also increased, while the arterio-venous difference became 16(11) and 10(3) (p = 0.04) mumol.litre-1, respectively. Left ventricular dP/dtmax increased by 22(7)% (p = 0.04) at the end of infusion. Thus, there seemed to be substantial uptake of inosine by the human heart, followed by improvement in haemodynamics.

Total ischaemic time and 9-year outcomes in STEMI patients treated with pPCI.

BACKGROUND: Prolonged total ischaemic time (TIT) has been shown to independently predict poor myocardial perfusion in STEMI patients and affect in-hospital mortality. We aim to evaluate the influence of TIT on long-term follow-up (F/U) and identify the factors associated with TIT in patients with STEMI treated with pPCI at a high volume centre. METHODS: In a prospective "all-comer" registry, clinical, angiographic and procedural characteristics, TIT and 9-year mortality were determined in consecutive STEMI patients treated with pPCI. Patients were divided according to TIT into three groups: A) <3, B) 3-6 and C) >6h. RESULTS: Among 1064 patients, TIT was known in 1002 patients, 5 patients were lost to F/U. For censored observations F/U was 7.2-8.8 years. There were 350, 461, and 186 patients in groups A, B, and C, respectively. Patients in group A compared to B and C were younger, more often males and smokers, less frequently had history of CAD, and more frequently had occluded infarct related artery. However, final TIMI3 was obtained more frequently. Overall 30-day mortality was 4%, one-year mortality 7% and nine-year mortality 27%. Multivariable logistic regression models indicated that longer TIT was associated with a higher risk of 9-year mortality (A-21%, B-28%, C-37%, p<0.0005). TIT>6h was independently associated with advanced age, diabetes mellitus, history of CAD and higher rate of initial TIMI grade flow 3. CONCLUSIONS: TIT is strongly related with mortality in STEMI patients even after nine years of F/U. This finding reinforces the necessity of shortening the TIT in all STEMI patients.

Decreased plasma dehydroepiandrosterone sulfate and dihydrotestosterone concentrations in young men after myocardial infarction.

Plasma levels of dehydroepiandrosterone sulfate (DHEA-S), testosterone, dihydrotestosterone (DHT) androstenedione, sex hormone-binding globulin (SHBG), lipoproteins, apolipoproteins and high density lipoprotein (HDL) subfraction were measured in 32 men aged 26-40 years after myocardial infarction (MI) suffered at least 3-4 months prior to the study, who were normocholesterolemic and had angiographically demonstrated coronary occlusion. The control group consisted of 76 healthy men aged 25-40 years. Blood samples were obtained in the morning from fasting subjects. A significant decrease in plasma DHEA-S and DHT levels were found in MI patients. Also, a significant decrease in HDL-cholesterol, HDL2-cholesterol (HDL2-C) and apolipoprotein A-I, an increase in apolipoprotein B and LDL-cholesterol (LDL-C) levels were observed in those patients as compared with healthy men. However, there were no differences in testosterone, androstenedione and SHBG concentrations between the groups. Significant correlations between testosterone and HDL2-C (r = 0.46, P less than 0.01), as well as between DHEA-S and HDL3-C (r = 0.39, P less than 0.05) levels in MI patients were observed. These results suggest that decreased levels of plasma DHEA-S and DHT may promote the development of coronary atherosclerosis in men.

Prior aspirin use predicts worse outcomes in patients with non-ST-elevation acute coronary syndromes. PURSUIT Investigators. Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy.

Aspirin is beneficial in the prevention and treatment of cardiovascular events, but patients who have events while taking aspirin may have worse outcomes than those not on aspirin. We investigated the association between prior aspirin use and clinical outcomes in 9,461 patients with non-ST-elevation acute coronary syndromes enrolled in the Platelet IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial, before and after adjustment for baseline factors. We also examined whether eptifibatide has a differential treatment effect in prior aspirin users. Prior aspirin users were less likely to have an enrollment myocardial infarction (MI) (vs unstable angina) (43.9% vs 48.8%, p = 0.001) but more likely to have death or MI at 30 days (16.1% vs 13.0%, p = 0.001) and at 6 months (19.9% vs 15.9%, p = 0.001). After adjustment, prior aspirin users remained less likely to have an enrollment MI (odds ratio 0.88, 95% confidence interval 0.79 to 0.97) and more likely to have death or MI at 30 days (odds ratio 1.16, 95% confidence interval 1.00 to 1.33) but not at 6 months (odds ratio 1.14, 95% confidence interval 0.98 to 1.33). In a multivariable model, eptifibatide did not have a different treatment effect in prior aspirin users compared with nonusers (p = 0.534). Prior aspirin users had fewer enrollment MIs but worse long-term outcomes than nonusers. We found no evidence for a different treatment effect of eptifibatide in prior aspirin users.

Management of ventricular septal defect with associated aortic incompetence.

Twenty-two patients with a ventricular septal defect and aortic incompetence underwent surgical repair. Mean age was 9.6 years (range, 9 to 15 years). Mean follow-up was 32.4 +/- 15.8 months. The ventricular septal defect was perimembranous in 19 patients and doubly committed or juxtaarterial in 3. Most showed only a small left-to-right shunt. Mean diameter was 11.9 +/- 4.8 mm. Aortic incompetence was mild in 6 patients, moderate in 4, and severe in 12. In 16 patients closure of the ventricular septal defect and aortic valvoplasty were both performed through the aortic root. There were no deaths. All patients retained normal sinus rhythm. No complete heart block was found. In 3 patients secondary aortic valve replacement was required for severe incompetence; in 1 the cause was bacterial endocarditis, in another technical failure, and in a third progressive incompetence over an 8-month period. All patients showed substantial clinical improvement, marked decrease or disappearance of the valvar incompetence, diminution of the left ventricular end-diastolic diameter, and decreased cardiothoracic ratio. We conclude that primary repair is the operation of choice for this combination of lesions. This can avoid or delay considerably valvar replacement. The left-sided approach proves safe and is our preferred technique.

Efficacy of trimetazidine in patients with recurrent angina: a subgroup analysis of the TRIMPOL II study.

OBJECTIVES: The revascularization procedures become more and more popular to treat coronary artery disease, in many countries. Some patients are free of angina after revascularization, without any documented re-stenosis present with recurrent angina symptoms after a period of time. The aim of this work was to assess the efficacy of trimetazidine in the subpopulation of patients with a history of PTCA or CABG, who were included in the TRIMPOL II study. METHODOLOGY: A subgroup of 94 patients was retrospectively analysed from the TRIMPOL II study, a multicentre, double-blind randomised placebo-controlled trial in 426 patients with stable effort angina. These patients have a history of revascularization for coronary artery disease, and they are still symptomatic after 6 months despite a treatment with metoprolol (50 mg twice daily). They were randomly allocated to receive either trimetazidine (20 mg 3 times daily) or placebo for 12 weeks, on top of the beta-blocker. Exercise test parameters, clinical efficacy and safety were assessed. Results were analysed using the Student test, the Mann-Whitney test or the Shapiro-Wilk test. RESULTS: Compared to placebo, the 12-week treatment with trimetazidine significantly improved: time to 1 mm ST segment depression (385.1 s +/- 144.6 s versus 465.0 s +/- 143.8 s [p < 0.01]); exercise test duration (466.9 s +/- 144.8 s versus 524.4 s +/- 131.5 s [p = 0.048]), total workload (9.0 m.e. +/- 2.4 m.e versus 10.1 m.e. +/- 2.4 m.e [p = 0.035]) as well as time to onset of angina (433.6 s +/- 164 s versus 508.1 s +/- 132.4 s [p = 0.031]). Weekly number of angina attacks and nitrate consumption were significantly reduced in the trimetazidine group when compared to placebo. Three mild gastro-intestinal side-effects were reported in the trimetazidine group. CONCLUSION: These results show that trimetazidine provides anti-anginal efficacy in post-revascularized patients with recurrent angina despite a monotherapy with metoprolol. The treatment was well accepted.

Immunophenotypic and functional characterization of peripheral blood mononuclear cell populations in patients with dilated cardiomyopathy.

Cell-mediated immune responsiveness was evaluated in 8 patients with dilated cardiomyopathy (CDM). The percentage of blood OKM1 (monocytes), OKT3 (T-cells), OKT4 (helper cells), OKT8 (suppressor cells) and Leu7 (NK) positive cells remained within the normal range whereas the percentage of Leu11 (NK) and OKIa1 (Ia determinant) positive cells was found to be decreased. The natural killer (NK) cell cytotoxicity was significantly lowered. The ConA-suppressor cell activity was seen to be enhanced while the responsiveness of lymphocytes to ConA was diminished. Thus, no consistent numerical changes in lymphocyte subsets were observed in patients with CDM. Some functional deficiencies were, however, detected, and it is possible that these may play a role in the pathogenesis of CDM.

Percutaneous mitral commissurotomy with the Inoue balloon for severe mitral stenosis during pregnancy.

Percutaneous mitral commissurotomy using the Inoue balloon was performed in seven pregnant women between May 1990 and November 1991. The mean age of the group was 31.5 years (range 28-35 years). The mean gestation time was 29 weeks (range 20-38 weeks). All patients presented with severe symptoms; two had a recent history of pulmonary oedema, the rest exhibited marked shortness of breath, and mild exercise and paroxysmal nocturnal dyspnea. All were in sinus rhythm. Two patients had previously undergone closed mitral valvulotomy five and 14 years before their recent hospitalization. Echocardiographic examination revealed severe mitral stenosis, with the mitral valve area being less than 1.2 cm2 in all but one patient. None of the patients had left atrial thrombi or mitral regurgitation as seen on two-dimensional and Doppler echocardiography. Four patients (two with restenosis) had severe lesions of the subvalvular apparatus with thickening and marked shortening of the chordae, as assessed by echocardiography. Successful percutaneous mitral valvulotomy was completed in all seven patients using 25-28 mm Inoue balloons. There was one, transient maternal complications. Fetal complication did not occur. It is concluded that percutaneous, transseptal, mitral balloon valvulotomy during pregnancy with the Inoue balloon is a safe procedure, which can be recommended for suitable clinical cases.

Long term follow up after percutaneous mitral commissurotomy with the Inoue balloon-incidence of restenosis.

UNLABELLED: The long term outcome of 300 consecutive patients following percutaneous mitral commissurotomy (PMC) with the Inoue balloon was analyzed with regard to the incidence of restenosis. There were 256 females and 44 males (mean age 44.4 +/- 9.9 years, range 18-69 years), 52 had previous surgical commissurotomy, 96 were in atrial fibrillation, and 16 had a history of embolism. PCM was carried out with a success rate of 84% (no significant mitral regurgitation and mitral valve area (MVA) > 1.5 cm2). Two hundred and seventy patients were available for clinical and serial echocardiographic studies at six months, 12 months and once a year thereafter (18 patients operated on for mitral regurgitation less than six months after PMC, three patients lost to follow up, nine patients refused to return). MVA increased with PMC from 1.18 cm2 +/- 0.3 to 2.0 +/- 0.3 cm2 and then decreased to 1.8 +/- 0.3 at a mean follow up of 24.0 +/- 13.5 months (range 6-55). Echocardiographic restenosis (RS) (MVA at follow up < 1.5 cm2 with a 50% loss of the initial gain) was found in 38 patients (14%). Twenty-five (66%) of them remained in NYHA class I or II. Restenosis free survival according to the Kaplan-Mayer curve was 93%, 86%, 77% and 73% at 12,24,36 and 55 months respectively. None of the 24 clinical, hemodynamic, echocardiographic or procedural variables used on the Cox proportional hazard regression analysis identified predictors of restenosis free survival. CONCLUSIONS: The overall incidence of echocardiographic restenosis post PMC is low (12.6%) in patients followed for a mean period of two years and often occurs without worsened clinical symptoms. It may be difficult to define clinical, echocardiographic or procedural factors as significant predictors of restenosis free survival.

Mechanical valve replacement in congenital heart disease in children.

BACKGROUND AND AIM OF THE STUDY: The study aim was to analyze predictive factors of long-term results after mechanical heart valve replacement in children. METHODS: Forty-four patients (19 males, 25 females; mean age 8.9+/-3.9 years, median 7.0 years, range: 1.3 to 15 years) underwent heart valve replacement with mechanical prostheses. Of these patients, 25 had left atrioventricular valve replacement (LavVR) (18 mitral, six tricuspid in corrected transposition of the great arteries (TGA), one common in a univentricular heart), 13 had aortic valve replacement (AVR) and six had tricuspid valve replacement (TVR). The etiology of the valvular disease was congenital in all patients, and complicated by infective endocarditis in seven (16%). Fifteen patients had undergone previous procedures and 16 required simultaneous repair of associated lesions. The mean size of the implanted prosthesis was 26 mm (range: 19-29 mm) for LavVR, 29.7 mm (range: 23-33 mm) for TVR, and 21.9 mm (range: 19-25 mm) for AVR. Postoperatively, all patients received oral anticoagulation. The mean follow up was 6.8+/-3.5 years (total 290 patient-years). RESULTS: There was no early mortality, but three patients (7%) died later; all late deaths occurred in patients with LavVR. There were two sudden deaths, both in patients with complex congenital heart disease and heart failure (before the ACE inhibitor era), and one valve-related death from thrombotic occlusion of a mitral prosthesis. Five patients were reoperated on; three for patient-prosthesis mismatch, one for periprosthetic leak, and one for aortic dissection due to Marfan's syndrome. Thrombotic obstruction occurred in three patients; two in the tricuspid position were treated successfully with thrombolysis, but one in the left atrioventricular position proved fatal. After seven years, the survival rate was 93.4%. CONCLUSIONS: Mechanical heart valve replacement in children aged over one year with congenital heart disease can be performed with satisfactory early and late results. Mechanical valves of >23 mm diameter in the atrioventricular position in the systemic ventricle, and >21 mm in the aortic orifice, can offer excellent long-lasting hemodynamic performance. However, mechanical valves in the tricuspid position are prone to develop thrombotic occlusion.

Long-term follow-up results of balloon valvuloplasty for congenital aortic stenosis: predictors of late outcome.

AIMS: Long-term follow-up of patients with aortic valve stenosis undergoing balloon valvuloplasty was evaluated with respect to survival, the need for repeat intervention and factors predicting late outcome. METHODS AND RESULTS: Forty-five patients between 3.5 to 23 years old (mean 11.7 +/- 4.5) were followed for 62 +/- 30 months (range 11-122). The transvalvar aortic gradient decreased from 84 +/- 20 to 36 +/- 10 mmHg (p < 0.001) and remained significantly lower (50 +/- 26 mmHg; p < 0.001) at follow-up. At that time, 10 patients (including 4 with significant valve incompetence) had gradients >/= 60 mmHg. The procedure resulted in significant valve incompetence (grade >/= 3) in 8 patients (17.8%). There was a progression of incompetence and 13 patients (28.9%) had significant regurgitation at follow-up. All survived. Fifteen patients (33.3%) required re-intervention 51 +/- 24 months after valvuloplasty. The indications were: aortic stenosis in 5 patients; regurgitation in 6 patients; and stenosis with regurgitation in 4 patients. Actuarial freedom from re-intervention at 2, 4, 6 and 8 years was 96%, 88%, 61% and 56% of patients, respectively. The residual post-valvuloplasty gradient was the only predictor of re-intervention for valve stenosis (odds ratio = 3.2 for every 10 mmHg gradient increase; p = 0.017). A residual post-valvuloplasty gradient >/= 40 mmHg increased the relative risk of re-intervention sixfold. The immediate post-valvuloplasty aortic regurgitation grade was the only risk factor of re-intervention for regurgitation (odds ratio = 34 for every incompetence degree increase; p = 0.0019). Incompetence grade >/= 2 increased the risk of re-intervention tenfold. CONCLUSIONS: Valvuloplasty carries the risk of development of valve incompetence, which progresses with time. Some patients develop restenosis. The

Light and electron microscopic picture of atherosclerotic plaque in stable and unstable angina.

By presenting this series of 127 cases of coronary atherectomy the authors join the workers who study morphological differences between the atherosclerotic plaques in stable and unstable angina. Routine staining of formalin-fixed, paraffin-embedded material was completed by the detection of T lymphocytes, macrophages, mast cells, smooth myocytes and grown-in capillaries using monoclonal antibodies (DAKO), as well as by the immunofluorescent demonstration of fibrinogen in the plaques. The plaques derived from patients with unstable angina showed a higher incidence of mast cells (significant) and macrophages (insignificant). These cells render the plaque more susceptible to rupture or fissuring. There was also significantly more frequent and quantitatively more abundant permeation of the plaque by fibrinogen that raises the chance of thrombosis. These findings support the view that unstable angina correlates with the phenomena that favour the rupture of the plaque and thrombosis. Electron microscopy has not been used so far to study coronary atherosclerotic plaques. This material includes 15 plaques from stable and 18 plaques from unstable angina. A cover of fibrin and blood platelets is a regular formation on the surface and in the superficial layer of the plaque from unstable angina. It contributes to the "thrombotic proneness" of the coronary artery. These plaques also show abundant elastic fibres. This pattern corresponds to myo-elastic intimal hyperplasia ("intimal thickening") where the production of intimal elastin constitutes an essential phenomenon. Intimal thickening is interpreted as a preatherosclerotic event. The presence of elastin reflects an early stage of the development of the plaque. The plaque from stable angina shows abundant collagen fibres, which aggravate the lesion.

The presence of Chlamydia pneumoniae in atherosclerotic plaques--a report of three cases of ischaemic heart disease.

The report presents three cases of ischaemic heart disease in which Chlamydia pneumoniae infections were detected first serologically, later the bacteria were shown in atherosclerotic plaques with electron microscopy, and finally C. pneumoniae strains were isolated from the tissues.

[Myocardial bridging as an isolated angiographic change in the anterior descending branch of the left coronary artery]. / Mostek miesniowy jako izolowana zmiana angiograficzna w galezi przedniej zstepujacej lewej tetnicy wiencowej.

Review of 1,900 cineangiograms revealed myocardial bridging in 15 patients. 6 patients with more than 75% systolic narrowing in LAD, no evidence of significant atherosclerotic coronary disease, and normal ventricular wall motion underwent further investigation which included clinical examination, ECG and exercise test. All patients suffered from uncharacteristic chest pain. Abnormal ECG showed no specific changes of ST segment. In 4 patients an exercise was positive. All investigated patients were treated with nifedipine. After 6 month therapy myocardial perfusion was evaluated by exercise radionuclide Th-201 myocardial scintigraphy. Normal perfusion was stated in 2 patients. In 4 others perfusion deficits were observed in LAD distribution. Exercise test repeated during therapy was positive in 2 of cases. Chest pain was less severe in all treated patients and Ecg became normal in 2 of them.

[Aortic-left ventricular tunnel--description of two cases]. / Tunel aortalno-lewokomorowy--opis dwóch przypadków.

This is a very rare congenital anomaly, which clinically imitates aortic insufficiency and therefore should be kept in mind by the cardiologist. Only an early precise diagnosis and proper surgical treatment will result in a good long-term prognosis. We have diagnosed and treated two patients, four and five years old, referred to us with a diagnosis of aortic insufficiency. Our final assessment was based on an obligatory cine-angio study, since a certain percentage of patients with this anomaly have concomitant lesions in the cardio-vascular system, which should be precisely detected. A brief differential diagnosis and discussion concerning different surgical techniques are presented. In our two cases obliteration of the tunnel using a Dacron patch inserted vertically in the tunnel with closure of both ostia was performed. This technique seems to be superior compared to the previous one in terms of preventing the progressive destruction of the aortic valve. All the authors agree that early surgical treatment is indicated before the left ventricle becomes dilated and the aortic valve significantly damaged. Two years post surgery our patients are in very good condition with: no signs and heart failure, a gradual diminution of the left ventricular cavity and satisfactory function of the aortic valve.