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I. The actual data base on the decision-making process of indication for revascularization reveals that angiographic severity of coronary artery disease (CAD) is the primary determinant of referral to coronary interventional procedures. Several recent studies demonstrated that after an acute myocardial infarction, women undergo cardiac catheterization to a lesser extent than men. Data of the MITI study and of the Cooperative Cardiovascular Project suggested that during acute treatment of myocardial infarction a somewhat less aggressive therapy is performed in women as compared to men. II. With respect to sex-related differences in the early and late outcome after elective PCI, the main problem is the small, limited amount of data due to the lack of randomized clinical studies including a larger number of women. The vast majority of data was obtained in patients with PTCA and stents. All the older studies and registers until 1993 revealed a three times higher periprocedural complication rate and in-hospital mortality in women. In recent studies such as BARI, after successful PCI women have an excellent long-term prognosis comparable or even better than in men. III.1. Several studies on the effect of interventional strategies in patients with unstable angina or non-ST elevation myocardial infarction NSTEMI) revealed superiority of an early invasive versus a more conservative, noninvasive approach. However, the data of the FRISC II and RITA-3 trials indicated that an early intervention strategy resulted in a beneficial effect only in men which was not seen in women. On the other hand, two studies (e.g., the TACTICS-TIMI- 18 study) showed an improved outcome of women with acute coronary syndrome after early invasive therapy. III.2. In numerous investigations, a higher early mortality after acute ST elevation myocardial infarction (STEMI) has been observed in women compared to men. Although placebo-controlled randomized trials of thrombolytic therapy have demonstrated a 25-30% reduction in early mortality, in-hospital survival has remained consistently lower for women than men after thrombolytic reperfusion. -- In our clinic, prospective studies on clinical events during the early phase (30 days) and during long-term follow-up for 4 years after direct (primary) PTCA for acute STEMI were performed in women. Data were obtained in 204 consecutive and unselected women; results in women were compared with those of 577 consecutive and unselected men who had undergone direct angiography/primary PTCA for acute STEMI in the same time span. PTCA of the infarct-related artery was equally successful in both sexes (women 95%, men 94%). In the group of patients with acute STEMI who had been treated with primary infarct PTCA, no difference of early (30 days) mortality was detected in women versus men. Total cumulative mortality during 4 years of follow-up was 12.5%, 14.5%, 18% and 23% in women, respectively, versus 9%, 10.5%, 12% and 15%, respectively, in men. The general trend for a higher postdischarge mortality in women became apparent after 3 years and reached significance after 4 years. After multivariate analysis, female gender was no independent risk factor of increased mortality. Thus, direct (primary) coronary angiography and PCI eliminate significant gender-specific differences in survival early after acute myocardial infarction. Long-term follow-up (4 years) also revealed no sex-related differences in mortality and cardiac morbidity after direct (primary) PCI for acute ST elevation myocardial infarction.

Eine 73-jahrige ubergewichtige Patientin hatte sich bei koronarer Zweigefaserkrankung 11/1995 einer aortokoronaren Bypassoperation mit Anlage eines linksseitigen Mammariabypasses auf den Ramus interventrikularis anterior der linken Koronararterie unterzogen. Die rechte Koronarie und der Ramus Circumflexus wurden im weiteren Verlauf wegen hamodynamisch relevanter Stenosen 2 und 3/2002 mittels Ballonangioplastie dilatiert. Wegen belastungsabhangiger Angina pectoris wurde die Patientin unter dem Verdacht der Rezidivstenose zur Herzkatheteruntersuchung 9/2002 stationar aufgenommen. Bei der korperlichen Untersuchung war rechtsseitig ein Blutdruck von 160/80 und linksseitig von 120/80 mmHg messbar. Die Koronarangiographie zeigte die seit 2/2002 bekannte koronare Dreigefaserkrankung mit einer Rezidivstenose der rechten Koronararterie, die in gleicher Sitzung mittels Ballondilatation und Stentimplantation behandelt wurde. Die Farbduplexsonographie der A. subklavia und der Carotiden zeigte neben ausgepragter Plaquebildung einen reduzierten Fluss der A. vertebralis links. Die linke A. subklavia war nur distal des Abgangs der A. vertebralis und mit poststenotischem Flussprofil darstellbar. Schon 2 Tage nach Dilatation und Stentimplantation bot die Pat. Angina pectoris bei der Korperwasche. Es zeigten sich neu aufgetretene EKG-Veranderungen. In der Kontrollkoronarangiographie konnte eine Rezidivstenose ausgeschlossen werden, es fiel eine ca. 70%-Stenose der linken A. subklavia mit einem ausgepragten Mammaria-Steal-Phanomen auf. Nach perkutaner transluminaler Angioplastie und Stentimplantation in die stenosierte A. subklavia links 10/2002 war die Pat. vollig beschwerdefrei. Nach aortokoronarer Bypass-Operation mit Mammaria-Graft kann bei trotz erfolgreicher Koronarrevaskularisation fortbestehender Angina pectoris ein Koronararterien- Steal-Syndrom ursachlich sein. In jedem Fall sollte bei der klinischen Aufnahmeuntersuchung der Blutdruck beidseits gemessen werden, um eine mogliche Subklavia-Stenose zu erkennen.

Prospektive, systematische Untersuchungen zur Pathophysiologie und zum Verlauf des akuten Myokardinfarktes (MI) nach direkter Angioplastie bei pramenopausalen Frauen und im Vergleich dazu bei jungen Mannern liegen bisher nicht vor. Methodik und Resultate: Es wurden insgesamt 782 konsekutive und unausgewahlte Patienten mit akutem ST-Hebungs-MI und einem Symptombeginn vor

Methodik: Analyse der Langzeitergebnisse der direkten PTCA bei 204 konsekutiven und unselektierten Frauen und 577 Mannern mit akutem Myokardinfarkt. Ergebnisse: Frauen waren im Durchschnitt alter, hatten eine bedeutsamere Komorbiditat und hatten eine langere Prahospitalphase als Manner. Die PTCA des Infarktgefases war erfolgreich bei 95% der Frauen und 94% der Manner. Die kumulative Gesamtmortalitat wahrend der ersten 4 Jahre war 12,5%, 14,5% 18% und 23% bei Frauen und 9%, 10,5%, 12% und 15% bei Mannern (p=ns bis Jahr 3, p

Um Pravalenz und klinische Bedeutung der Kollateralzirkulation zu Myokard distal eines akuten Koronarverschlusses zu untersuchen, wurden Koronarangiogramme von konsekutiven und unselektierten Patienten mit akutem Myokardinfarkt vor jeglicher Reperfusionstherapie analysiert und mit klinischen Daten korreliert. Methodik Bei 700 konsekutiven und unselektierten Patienten mit akutem ST-Hebungsinfarkt wurde im Mittel nach 3,7±3 Stunden (0,5–12) ein Koronarangiogramm ohne vorangehenden Thrombolyseversuch angefertigt. Bei 626/700 Patienten (89%) lag ein kompletter Koronargefasverschluss vor. Bei diesen Patienten wurde die Kollateralzirkulation klassifiziert. Der Kollateralisierungsgrad wurde mit klinischen Befunden, dem Verlauf nach 30 Tagen und der globalen und regionalen Wandbewegung korreliert. Ergebnisse Kollateralen waren bei 334/626 Patienten (69%) nachweisbar, bei 242 Patienten (38%) ein Kollateralfluss Grad 2 oder 3. Bei Frauen gegenuber Mannern und bei Patienten mit einer Mehrgefaserkrankung wurden haufiger Kollaterale gefunden. Die Pravalenz von Kollateralen war von Alter und Diabetes mellitus unabhangig. Patienten, die innerhalb von 3 Stunden nach Symptombeginn angiographiert werden konnten, hatten weniger haufig Kollateralen als nach >>;6 Stunden angiographierte Patienten (66% vs. 75%, p

In einer prospektiven Studie wurde die Schilddrusenstoffwechsellage bei 102 Patienten, welche sich einer Koronarangiogaphie unterziehen mussten, unter Berucksichtigung der Schilddrusenmorphologie untersucht. Vor der intraarteriellen Kontrastmittelgabe und drei Wochen nach dem Eingriff wurden die Serumkonzentrationen von „TT3, rT3, TT4, fT4 und TSH“ sowie die Urinjodausscheidung gemessen. In die Untersuchung wurden nur Patienten mit euthyreoter Schilddrusenfunktion eingeschlossen, um die Frage zu beantworten, ob und in welchem Ausmas die intraarterielle Gabe nichtionischen jodhaltigen Kontrastmittels die Schilddrusenfunktion bei euthyreoten Patienten in Abhangigkeit von der Schilddrusenmorphologie beeinflusst und ob die Schilddrusenmorphologie einen prognostischen Faktor fur das Hyperthyreoserisiko darstellt. Es wurde eine Ultraschalluntersuchung der Schilddruse durchgefuhrt und der Autoantikorperstatus (TPO-Ak, TG- Ak, TSH-Rezeptor-Ak) der Patienten ermittelt. Entprechend der Ultraschallbefunde wurden 4 verschiedene Schilddrusenmorphologien unterschieden: normale Schilddrusen (n=37), normal grose knotig veranderte Schilddrusen (n=16), diffuse Strumen (n=15) und Knotenstrumen (n=34). 25 Patienten wiesen TG-Ak auf, 13 Patienten TPO-Ak. Bei keinem der Patienten waren TSH-Rezeptor-Antikorper nachweisbar. Die Serumspiegel von TT3 anderten sich nicht signifikant nach der Jodgabe (p=0,30), wahrend TT4 und fT4 signifikante Veranderungen in allen 4 morphologischen Gruppen zeigte (fT4 p

Bei Patienten mit operativer Myokardrevaskularisation kann es spat postoperativ (erneut) zu einem Myokardinfarkt kommen. Ob es dabei vorwiegend zum Bypass- oder Nativgefasverschlus kommt, ist bei diesen Patienten nicht genau bekannt. Uber angiographische Untersuchungen hierzu und/oder systematische direkte, kathetergestutzte Rekanalisationsversuche wurde bei diesen Patienten bisher nicht berichtet. Wir fertigten deshalb bei einer konsekutiven Gruppe von 21 Patienten mit akutem Myokardinfarkt und stattgehabter aortokoronarer Bypassoperation akute Koronarangiogramme an. Ziel der Untersuchung war einerseits die Analyse der vorherrschenden Infarktursache bei operierten Patienten und anderseits die Steuerung einer individuellen Rekanalisationsstrategie bei diesen Patienten. Bei 12/21 Patienten wurde der Infarkt am ehesten durch einen akuten Bypassverschlus hervorgerufen. Eine intrakoronare Fibrinolyse und/oder direkte PTCA von Bypassgefasen war erfolgreich bei 6/8 Patienten, von Nativgefasen bei 1/2 Patienten, und bei jeweils 1 Patienten wurde eine sofortige, erneute Bypassoperation durchgefuhrt bzw. konservativ behandelt. Bei 9/21 Patienten war der Infarkt durch einen Verschlus eines ungeschutzten Nativgefases verursacht. Die direkte PTCA dieser Nativgefase war bei 6/7 Patienten erfolgreich, bei ebenfalls jeweils 1 Patienten wurde eine sofortige, erneute Bypassoperation durchgefuhrt bzw. konservativ behandelt. Insgesamt war ein kathetergestutzter Rekanalisationsversuch bei 13/17 Patienten erfolgreich. Die 30-Tage- bzw. 1-Jahres-Mortalitat nach Entlassung war 5% (1/21 Patienten) bzw. 12%. Die linksventrikulare Auswurffraktion betrug 46% vor Entlassung. Zusammenfassend sind bei operierten Patienten der akute Bypass-Verschlus und der Verschlus einerr nativen, nicht bypassgeschutzten Koronararterie zu je etwa der Halfte Ursache akuter Myokardinfarkte. Bei invasivem, individuell angepastem, rekanalisierendem Vorgehen scheint die Hospitalmortalitat dieser Patienten niedrig zu sein.

Coronary atherectomy specimens from 50 patients with coronary heart disease were examined for the presence of Chlamydia pneumoniae by two different methods of polymerase chain reaction (PCR) and by in situ hybridization. C. pneumoniae DNA was detected by PCR in atherosclerotic plaques of four patients (8%). Two patients' coronary atheromas were positive, both by a single-step 16S rRNA-based PCR and by an omp1-based nested PCR. The other two patients' specimens were positive only by the nested PCR. In contrast, C. pneumoniae was not detected by in situ hybridization in any of the cardiovascular tissues tested. Of three patients with evidence of C. pneumoniae in coronary atheromas, two had an antibody titer of 1:32 and the third had no specific antibodies detectable. Results of this study demonstrate a low prevalence of C. pneumoniae DNA in coronary atheromas. These findings do not support the hypothesis that the organism plays a major role in atherogenesis.

The purpose of this study was to analyze long-term follow-up information over several years from consecutive, unselected patients treated with direct percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction (MI).Direct PTCA is often used in patients with acute MI. Short-term results are favorable. However, there is less information available on long-term observations over several years in these patients.A total of 416 consecutive and unselected patients with acute MI underwent direct PTCA. Survival of the acute infarct phase was 94.2%; the remaining 392 patients--the study population-were discharged and followed for 3.3+/-1.4 years. Mortality as well as cardiac events and reinterventions are reported. Clinical variables assessed at the time of discharge are submitted to statistical analysis to detect potential risk factors.Total cumulative mortality in the first year was 10% for the entire group and 6% for patients not presenting in cardiogenic shock. Mortality after discharge was 4.6% in the first year and dropped to4% per year thereafter. Reinterventions after discharge were required in 16% in the first year and in4% per year in years 2 to 4. Poor left ventricular ejection fraction (35%), three-vessel disease and advanced age (or =75 years) were long-term risk factors for total mortality after direct PTCA.The clinical benefit of direct PTCA for acute MI is maintained during follow-up with respect to mortality. However, reinterventions for restenosis or de novo stenosis are often required (10% to 20%). Although few in number (10%), patients with severely impaired left ventricular function continue to have a poor prognosis.

Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagonists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).

A review of the literature suggests that direct PTCA for acute myocardial infarction is indicated and feasible in 90-95% of unselected, consecutive patients; direct PTCA is reported to be successful in > 90% of procedures. This results in a hospital mortality of 3-7% for unselected patients and a 4% re-infarction rate. A recent meta-analysis of direct PTCA vs i.v. thrombolysis in patients with acute infarction demonstrates a lower mortality after PTCA (4.4% vs 6.5%, p = 0.02) as well as lower mortality/re-infarction rate (7.2% vs 11.9%, p < 0.001). Mortality in the 1st year after discharge is < 5% with about half of the fatalities being due to cardiac causes. Patients presenting with or developing cardiogenic shock in the acute infarct phase experience a 20-50% acute mortality. Mortality rests at < 10% in these patients in the first year after discharge. In conclusion, (1) direct PTCA is feasible without additional risks in patients with acute myocardial infarction, (2) angiographic and clinical success rates of direct PTCA are favorable and superior to i.v. thrombolysis in the hands of expert operators, and (3) referral to an institution providing the option of immediate, direct PTCA must be considered in the patient with acute infarction but contraindication(s) to i.v. thrombolysis.

Despite theoretical advantages of Directional Coronary Atherectomy (DCA) vs. PTCA, the first two controlled studies comparing both methods, the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT), and the Canadian Coronary Atherectomy Trial (CCAT), showed no clinical benefit of DCA, A second generation of trials, the Optimal Atherectomy Restenosis Study (OARS) and the Balloon versus Optimal Atherectomy Trial (BOAT), designed to optimize DCA with the use of 7F devices and adjunctive PTCA revealed lower angiographic restenosis rates compared to CAVEAT. In addition, the preliminary follow-up results of BOAT, presented by Donald S. Baim in Birmingham in August 1996, showed a 20% reduction of angiographic restenosis after DCA compared to PTCA. There was no association between post-procedure CK-MB elevation in the DCA group and late mortality. These results may further expand the application of DCA to clinical routine, whereas this procedure still has specific indications like treatment of ostial and bifurcation lesions and atherectomy in future may be the treatment of choice for restenosis in coronary stents.

Plasma and tissue concentrations of the angiotensin-I converting enzyme (ACE) have been shown to be associated with the ACE insertion/deletion (I/D) polymorphism. The purpose of this study was to examine the relation of ACE levels in atherosclerotic plaques to the ACE I/D polymorphism and to restenosis after balloon angioplasty and directional atherectomy (DCA). The study included 104 patients who underwent DCA and received angiographic follow-up at 12 to 18 months. The amount of ACE protein in various morphologically defined plaque components (fibrous, atheromatous, and complicated lesions) of the atherectomy specimens was determined by qualitative and semiquantitative immunohistochemistry. ACE levels were related to the ACE genotype, to plaque morphology and to the risk of restenosis. Sequential staining revealed that pathologic ACE overexpression of the atherosclerotic lesions occurred in intimal smooth muscle cells, fibrocytes/fibroblasts and macrophage/foam cells. The ACE content of the whole plaques and of the single plaque components was not associated with the I/D polymorphism, but with restenosis after coronary interventions. In addition, ACE levels in the atherosclerotic lesions correlated with the severity of vessel wall damage. The ACE phenotype might serve as an indicator for the risk of restenosis after coronary interventions.

Summary Background: Fibrinogen has been demonstrated to be an independent risk factor of cardiovascular disease. The absence of the Haelll cutting site (H2 allele) of an H1/H2 gene variation in the promoter region of the (β fibrinogen gene was associated with increased levels of fibrinogen. Methods and Results: In the present study, the effects of the H1/H2 gene variation not only on plasma fibrinogen concentrations but also on coronary artery disease (CAD) and myocardial infarction (MI) were investigated in 923 individuals who underwent coronary angiography for diagnostic purposes. Relation of the H1/H2 genotype to fibrinogen plasma levels: A strong association was observed between the H1/H2 gene variation and fibrinogen levels. The differences in fibrinogen plasma levels between H2H2 and H1H1 homozygotes were almost threefold more pronounced within subjects with clinical chemical signs of an acute phase reaction (CRP ≥ 7.5 mg/1) than within a subgroup of subjects without these signs (CRP < 7.5 mg/1) (median of CRP distribution: 7.5 mg/1). In 207 patients who underwent aortocoronary bypass surgery plasma fibrinogen levels were almost identical directly after surgery. Two days after operation fibrinogen increased to clearly higher levels in H2H2 homozygotes than in H1H2 and H1H1 genotypes, whereas almost the same maximal increases in fibrinogen concentrations were reached 3-4 days after surgery in all individuals. Relation of the H1/H2 genotype to CAD and MI. Whereas in the total population the plasma fibrinogen concentrations were strongly associated with smoking, CAD and MI, an association of the H1/H2 gene variation to CAD and MI was not detected. However, mean age at first MI of H2H2 individuals (62.9 years) was clearly higher than of H1H2 genotypes (56.9 years) and of H1H1 subjects (56.4 years). In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoAl plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although – also in these high risk groups – mean age at first MI of H2H2 individuals were higher than of the other two genotypes. Conclusions: Obviously, the H2 allele of the fibrinogen H1/H2 genotype does not only influence basal fibrinogen concentrations, but particularly also the extent of fibrinogen level increase during acute phase reaction. Whereas the fibrinogen plasma level is positively associated with coronary artery disease and myocardial infarction, the H2 allele - although exhibiting an association with elevated fibrinogen levels - was not positively associated with CAD and MI.

Background An insertion/deletion (I/D) polymorphism of the angiotensin I–converting enzyme (ACE) gene has been postulated to be associated with an increased risk of coronary artery disease (CAD) and myocardial infarction (MI). Methods and Results In the present study, the effects of I/D gene polymorphism and of ACE activity on CAD and MI were investigated in 920 individuals who underwent coronary angiography for diagnostic purposes. In the total population and in all CAD and MI groups, a strong association was observed between the gene polymorphism and ACE activities; DD genotypes had approximately twofold higher ACE activities than II genotypes. Although classic risk and protective factors of CAD and MI were identified, associations of ACE genotype and of ACE activity to CAD and MI were not detected in the total population. Among subjects defined to be at lower risk of MI by low body mass index and low cigarette consumption, however, an association of the DD genotype with MI was found. Exclusion of individuals with triglyceride levels >140 mg/dL and cholesterol levels >180 mg/dL revealed an association of the DD genotype with CAD. An association of the ACE activity with CAD or MI could not be demonstrated in any of the low-risk populations. Conclusions Increased ACE activity obviously is not a risk factor of CAD or MI. The importance of the deletion polymorphism for the development of CAD and MI may be restricted to individuals without classic risk factors.

Systemic and coronary haemodynamic effects of carbochromen (0.125 mg kg-1 min-1 for 40 min i.v.) and dipyridamole (0.05 mg kg-1 min-1 for 10 min i.v.) were investigated in 18 patients without detectable heart disease. Both drugs induced a comparable increase in coronary blood flow (carbochromen: from 82 +/- 23 to 337 +/- 68 ml.100 g-1.min-1; dipyridamole: from 78 +/- 9 to 301 +/- 61 ml.100 g-1.min-1). This resulted in a minimal coronary resistance of 0.23 +/- 0.04 mmHg.ml-1.100 g.min for dipyridamole and of 0.24 +/- 0.04 mmHg.ml-1.100 g.min for carbochromen. In response to dipyridamole (n = 12) heart rate increased from 73 to 94 beats min-1 (P less than 0.005) and mean aortic pressure fell from 89 to 78 mmHg (P less than 0.001). After administration of carbochromen (n = 6) no significant systemic effects occurred. Dipyridamole induced a significant increase in myocardial oxygen consumption by 46% (P less than 0.001); after application of carbochromen myocardial oxygen consumption remained unchanged. From these data it can be concluded that for the evaluation of coronary dilatory capacity carbochromen may be more suitable than dipyridamole because (1) maximal coronary vasodilation is induced without changes in myocardial oxygen consumption and (2) no systemic effects occur.

Summary A total of 38 consecutive patients with acute myocardial infarction (MI) ineligible to i.v. thrombolysis underwent immediate, selective coronary angiography. Thereafter, percutaneous transluminal coronary angioplasty (PTCA) of the occluded artery was attempted if the infarct-related vessel showed TIMI 0, I, or II-flow. All patients were ineligible to i.v. thrombolysis because of advanced age (80 years) or increased risk of bleeding complications. TIMI-flow III was restored in 35/38 patients (92%) with a residual stenosis of

A 73-year-old obese woman underwent coronary artery-bypass operation in 11/1995 because of a coronary two vessel disease. The left coronary artery was bypassed by the left mammarial internal artery. In 2 and 3/2002, balloon-dilatation of stenoses of the right coronary artery and the circumflex was performed. Angina pectoris relapsed and in 9/2002 the patient was admitted to our hospital with tentative diagnosis of restenosis. Physical investigation showed a blood pressure of the right arm of 160/80 and of the left arm of 120/ 80 mmHg. Coronarography showed the three vessel disease known since 2/2002 with a restenosis of the right coronary artery which was immediately treated by balloon-dilatation and stent-implantation. Colour duplex-sonography of the carotid and subclavian arteries revealed extraordinary plaques and a reduced flow of the left vertebral artery. The left subclavian artery could only be seen distal to the discharge of the vertebral artery and showed a poststenotic flow. The patient had angina pectoris when carrying out personal hygiene already 2 days after balloon-dilatation and stent-implantation. ECG showed new aspects. Coronarography showed no relapse of stenosis, but 70% stenosis of the left subclavian artery with a marked coronary-steal-syndrome. In 10/ 2002, the patient underwent balloon-dilatation and stent-implantation of the subclavian stenosis and became free of complaints. Coronary-steal-syndrome can be the reason for persistent angina pectoris in spite of successful coronary artery-bypass operation with a mammarial internal bypass. It is absolutely necessary to take blood pressure from both arms to recognise a possible stenosis of the subclavian artery which can be the key to all.

Prospective, systematic studies of the pathophysiology and prognosis of premenopausal women vs young men who suffer an acute myocardial infarction (MI) and are treated with direct angioplasty are scarce.A total of 782 consecutive and unselected patients who presented with an acute ST-elevation MI within 12 h of symptom onset underwent immediate angiography to guide direct angioplasty. Using this therapeutic approach clinical characteristics, angiographic observations, and short- and long-term prognosis were analyzed in a sub-group of 31 premenopausal women and compared to 192 young men with acute MI. Premenopausal women account for 4% of individuals with acute MI and for 15% (31/205) of all women. Men of the same age range make up 25% (192/782) of all MI patients (p0.001). Three or more classic risk factors were present in 20/31 women. Young women presented later than men. Angiography demonstrated a coronary occlusion in 27/31 women (88%) but in 98% of young men (p0.02). Direct PTCA was successful in all premenopausal women and in 179/185 men (97%, p=ns). Predischarge EF was 57% in women and 54% in men (p=ns). After 4 years of follow-up, all women had survived as compared to a 95% survival in young men. Major cardiac events had occurred in 50% of persons of either gender.Premenopausal women account for 4% of individuals and for 1/6 of all female patients who presented with acute MI within 12 h of onset. Hospital admittance is delayed in young women. MI was caused by (atherosclerotic) coronary occlusion in most young women and in virtually all young men. Short- and long-term survival of premenopausal women is favorable after direct PTCA for acute MI and not different than men from the same age group.

Long-term follow-up of 204 consecutive and unselected women vs 577 men after direct PTCA for acute myocardial infarction.Women were older, had more significant comorbidity, and had a longer prehospital phase. Direct PTCA of the infarct artery was angiographically successful in 95% of women and in 94% of men. Total cumulative mortality during 4 years of follow-up was 12.5%, 14.5% 18%, and 23% in women, respectively, vs 9%, 10.5%, 12%, and 15%, respectively, in men (p=ns through year 3, p0.05 thereafter). After multivariate analysis, gender was no independent risk factor of increased mortality. Major cardiac events and need for target vessel revascularization were unrelated to gender.There are no gender-specific differences in mortality after direct PTCA for acute myocardial infarction.

Angiograms from consecutive and unselected patients with acute myocardial infarction were studied with respect to the prevalence as well as the significance of coronary collateral circulation to myocardium distal to the acute coronary occlusion.Coronary angiograms were obtained from 700 consecutive and unselected patients with an acute transmural infarction within 3.7 +/- 3 hours (0.5-12) of symptom onset. No patient had undergone i.v. thrombolysis prior to angiography. Complete and acute vessel occlusion was found in 626/700 patients (89%). Coronary collaterals were detected and graded using Rentrop's classification. The grade of collateral circulation was related to the clinical course after 30 days and to the global and regional left ventricular wall motion.Collaterals were found in 334 patients (69%); 242 patients (38%) had collateral flow grade 2 or 3. Collaterals were demonstrated more frequently in women vs men and in patients with multivessel disease. The prevalence of collaterals was unrelated to age and the presence of diabetes mellitus. Patients who had angiography within 3 hours of symptom onset had collaterals detected less frequently than patients who had angiography beyond 6 hours (66% vs 75%, p0.05). No collaterals were found in 17/37 patients (47%) in cardiogenic shock and inferior MI but in only 30/164 patients (18%, p0.01) without shock. Global and regional left ventricular wall motion after 2 weeks was unrelated to the degree of coronary collateral circulation during acute myocardial infarction.Collateral circulation to myocardium distal to an acutely occluded coronary artery is detected in 2/3 patients during the acute infarct phase. The absence of collaterals is related to the early occurrence of cardiogenic shock in patients with inferior MI but not to the presence of diabetes mellitus. After direct angioplasty of the infarct vessel, the protective effects of coronary collaterals on chronic LV function remain uncertain.

In a prospective study, thyroid metabolism in 102 patients undergoing diagnostic coronary angiography was investigated, stratified for thyroid morphology. The thyroid function serum parameters "TT3, rT3, TT4, fT4 and TSH" and the urinary iodine excretion were measured before and three weeks after diagnostic intraarterial administration of the iodine-containing contrast agent. Only patients with euthyroid function were included in order to answer the questions whether or not the administration of non-ionic iodine containing contrast medium leads to significant thyroid function changes in euthyroid patients and whether thyroid morphology is a prognostic factor for the risk of developing hyperthroidism. Serum concentrations of thyroid autoantibodies (TPO-Ab, Tg-Ab, TSH-receptor-Ab) were measured and thyroid ultrasound was performed. According to the ultrasound findings, 4 morphologic groups were formed: normal thyroid glands (n = 37), normal sized but nodular glands (n = 16), diffuse goiter (n = 15) and nodular goiter (n = 34). Twenty-five patients were positive for Tg-Ab; TPO-Ab were found in 13 patients. TSH-receptor-Abs were not detected in all patients. TT3 levels did not significantly change after iodine application (p = 0.30). TT4 and fT4 levels showed significantly different alterations in the 4 groups (fT4 p0.001). The amount of iodine given did not influence alteration of serum concentrations of TSH (p = 0.67), TT3 (p = 0.68), TT4 (p = 0.37), fT4 (p = 0.92) and rT3 (p = 0.81). Elevated levels of urinary iodine excretion correlated with the amount of contrast medium given (p = 0.087). Albeit there was a high number of nodular transformed glands and goitrous patients included, and our cohort was recruited in an iodine deficient area, we did not observe hyperthyroidism in any patient. However, thyroid function parameters are significantly altered after coronary angiography independent of antibody status and the amount of contrast agent given, but dependent on thyroid morphology.

Kardiovaskulare Erkrankungen stellen die haufigste Todesursache bei Frauen und Mannern in den westlichen Industrienationen dar. In den USA z. B. stirbt ein Drittel der Frauen an der koronaren Herzkrankheit (250 000 Todesfalle pro Jahr). Frauen weisen vor der Menopause offenbar einen biologischen Schutz gegen die koronare Herzkrankheit auf, was sich in einem im Vergleich zu Mannern 10–12 Jahre spateren Auftreten der koronaren Herzkrankheit widerspiegelt [5, 20].

been performed using reduced voltage and acquisition of images only in diastole. A 50% reduction in radiation dose may be expected without compromise in image quality. Thus, MSCT angiography is a rapidly developing new imaging modality for visualizing the proximal and midsegments of the coronary arteries. Further technical advances to improve diagnostic accuracy and clinical usefulness are expected in the near future.

Whether acute and direct percutaneous transluminal coronary angioplasty improves the incidence of nonsustained ventricular tachycardia in patients surviving acute myocardial infarction is not known. In 400 consecutively studied patients, Lown classification IVb on Holter monitoring was only associated with arrhythmia morbidity, whereas reduced ejection fraction was related to total and cardiac mortality and arrhythmia morbidity.

Patients who have undergone coronary artery bypass grafting may develop acute myocardial infarction late after surgery. It is not exactly known in these patients whether acute infarction is predominantly caused by occlusion of bypass or native vessels. Also, there is no systematic and prospective data available with respect to an invasive, revascularizing therapeutic approach. Therefore, acute coronary angiograms were obtained in 21 consecutive patients with acute infarctions and remote bypass grafting to elucidate mechanisms causing myocardial infarction in these patients, and to assess results of catheter-based recanalization. Infarction was causes by acute graft occlusion in 12/21 patients. Fibrinolysis and/or PTCA of grafts was successful in 6/8 attempts, direct PTCA of a native vessel was effective in 1/2 patients, 1 patient underwent emergency re-CABG, and another patient was treated noninvasively. Occlusion of native, ungrafted vessel caused infarction in 9 patients. Direct PTCA of native vessels was effective in 6/7 of those patients, 1 patient had re-CABG, and another patients was treated non-invasively. Together, catheter-based recanalization was obtained in 13/17 attempts. Thirty-day and 1 year mortality (after discharge) was 5% (1/21 patients) and 12%, respectively. Predischarge ejection fraction was 46%. In conclusion, acute occlusion of bypass grafts is responsible for about half of all cases of myocardial infarction in patients late after surgery. Direct angiography and individually tailored catheter-based recanalization in patients with acute myocardial infarction late after surgery yield promising results.

OBJECTIVE: Mortality in diabetic patients with acute myocardial infarction (MI) is high. The significance of the pretreatment coronary status in type 2 diabetic patients with acute MI, as well as the effect of mechanical revascularization using percutaneous transluminal coronary angioplasty (PTCA), has not been established. RESEARCH DESIGN AND METHODS: All patients with type 2 diabetes and acute MI (n = 54) were prospectively enrolled into a study of immediate coronary angiography to guide PTCA of the occluded infarct vessel. Hospital and long-term course were assessed and compared with an unselected control group of nondiabetic patients (n = 358) who were enrolled in the same study. RESULTS: Angiography showed that sites of occlusion and acute coronary flow were similar in both groups. Multivessel disease and shock were more common in type 2 diabetic versus nondiabetic patients: 69 vs. 51% and 21 vs. 10% (P < 0.02), respectively. Direct PTCA was successful in > 90% in both groups. Mortality after 30 days was 13% in type 2 diabetic patients versus 5% in patients without diabetes (P < 0.04). Left ventricular (LV) ejection fraction before discharge was lower in diabetic patients (48 +/- 17 vs. 55 +/- 15%, P < 0.05). Mortality 1 year after discharge was 11 vs. 4% in diabetic versus nondiabetic patients (P < 0.02). Multivariate analysis identified type 2 diabetes as an independent risk factor for acute, but not for late, mortality. CONCLUSIONS: Direct PTCA is safe and effective in type 2 diabetic patients with acute MI. Mortality after 30 days in unselected diabetic patients is < 15% with this approach. Advanced disease and shock contribute to an increased mortality in type 2 diabetic patients with acute MI versus nondiabetic patients.

Coronary atherectomy specimens from 50 patients with coronary heart disease were examined for the presence of Chlamydia pneumoniae by two different methods of polymerase chain reaction (PCR) and by in situ hybridization. C. pneumoniae DNA was detected by PCR in atherosclerotic plaques of four patients (8%). Two patients' coronary atheromas were positive, both by a single-step 16S rRNA-based PCR and by an omp1-based nested PCR. The other two patients' specimens were positive only by the nested PCR. In contrast, C. pneumoniae was not detected by in situ hybridization in any of the cardiovascular tissues tested. Of three patients with evidence of C. pneumoniae in coronary atheromas, two had an antibody titer of 1:32 and the third had no specific antibodies detectable. Results of this study demonstrate a low prevalence of C. pneumoniae DNA in coronary atheromas. These findings do not support the hypothesis that the organism plays a major role in atherogenesis.

Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagonists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).

High-frequency ultrasound can provide high-resolution imaging for diagnosing diseases of the head and neck. Over the last few years, a virtual technical evolution has led to the development of small and flexible ultrasound transducers with even greater anatomic resolution. The aim of the present study was to evaluate the efficacy of this new technique for imaging normal and altered anatomical structures of the endolarynx. Specially developed high-resolution, real-time ultrasound transducers (10 and 20 MHz) placed on the tip of endoluminal catheters were inserted into 20 autopsied larynges and five laryngectomy specimens. In a standardized examination process the endolarynx was analyzed in a real-time mode. Using this technique, exact 360 degrees cross sections of the larynx were obtained, demonstrating that it was possible to image the structures of the endolarynx with ultrasonography. Depending on the frequency used, all anatomical structures could be visualized up to a depth of 2 cm. In laryngeal cancer the depth of tumor as well as its relationship to the laryngeal framework could be clearly recognized. These findings suggest that this new endoluminal sonographic procedure represents a potentially important diagnostic tool in the assessment of laryngeal carcinoma.

A review of the literature suggests that direct PTCA for acute myocardial infarction is indicated and feasible in 90-95% of unselected, consecutive patients; direct PTCA is reported to be successful in90% of procedures. This results in a hospital mortality of 3-7% for unselected patients and a 4% re-infarction rate. A recent meta-analysis of direct PTCA vs i.v. thrombolysis in patients with acute infarction demonstrates a lower mortality after PTCA (4.4% vs 6.5%, p = 0.02) as well as lower mortality/re-infarction rate (7.2% vs 11.9%, p0.001). Mortality in the 1st year after discharge is5% with about half of the fatalities being due to cardiac causes. Patients presenting with or developing cardiogenic shock in the acute infarct phase experience a 20-50% acute mortality. Mortality rests at10% in these patients in the first year after discharge. In conclusion, (1) direct PTCA is feasible without additional risks in patients with acute myocardial infarction, (2) angiographic and clinical success rates of direct PTCA are favorable and superior to i.v. thrombolysis in the hands of expert operators, and (3) referral to an institution providing the option of immediate, direct PTCA must be considered in the patient with acute infarction but contraindication(s) to i.v. thrombolysis.

Fibrinogen has been demonstrated to be an independent risk factor of cardiovascular disease. The absence of the HaeIII cutting site (H2 allele) of an H1/H2 gene variation in the promoter region of the beta fibrinogen gene was associated with increased levels of fibrinogen.In the present study, the effects of the H1/H2 gene variation not only on plasma fibrinogen concentrations but also on coronary artery disease (CAD) and myocardial infarction (MI) were investigated in 923 individuals who underwent coronary angiography for diagnostic purposes. Relation of the H1/H2 genotype to fibrinogen plasma levels: A strong association was observed between the H1/H2 gene variation and fibrinogen levels. The differences in fibrinogen plasma levels between H2H2 and H1H1 homozygotes were almost threefold more pronounced within subjects with clinical chemical signs of an acute phase reaction (CRPor = 7.5 mg/l) than within a subgroup of subjects without these signs (CRP7.5 mg/l) (median of CRP distribution: 7.5 mg/l). In 207 patients who underwent aortocoronary bypass surgery plasma fibrinogen levels were almost identical directly after surgery. Two days after operation fibrinogen increased to clearly higher levels in H2H2 homozygotes than in H1H2 and H1H1 genotypes, whereas almost the same maximal increases in fibrinogen concentrations were reached 3-4 days after surgery in all individuals. Relation of the H1/H2 genotype to CAD and MI. Whereas in the total population the plasma fibrinogen concentrations were strongly associated with smoking, CAD and MI, an association of the H1/H2 gene variation to CAD and MI was not detected. However, mean age at first MI of H2H2 individuals (62.9 years) was clearly higher than of H1H2 genotypes (56.9 years) and of H1H1 subjects (56.4 years). In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoA1 plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although-also in these high risk groups-mean age at first MI of H2H2 individuals were higher than of the other two genotypes.Obviously, the H2 allele of the fibrinogen H1/H2 genotype does not only influence basal fibrinogen concentrations, but particularly also the extent of fibrinogen level increase during acute phase reaction. Whereas the fibrinogen plasma level is positively associated with coronary artery disease and myocardial infarction, the H2 allele-although exhibiting an association with elevated fibrinogen levels-was not positively associated with CAD and MI.

In 11 rats, the microcirculation of the repeatedly ischaemic (stunned) left ventricular myocardium was studied using in vivo fluorescence microscopy. Stunning was provoked by six subsequent 10 min ligations of the left anterior descending coronary artery, each of them followed by a 20 min reperfusion period. In the stunned myocardium showing hypokinetic wall motion, myocardial blood flow dropped by 55%; in this region, leukocytes often appeared in slow-flow capillaries plugging capillary branches. Closely linking to leukocyte adherence, a rise of microvascular permeability was documented by extravascular clouds of fluorescent dextran. After nifedipine treatment, in ischaemic regions marked dilatation of larger A1 and A2 arterioles was noted, in addition to the ischaemia-induced dilatation of smaller A3 and A4 arterioles. Furthermore nifedipine and nisoldipine reduced the number of adherent leukocytes in post-capillary venules and capillaries of the repeatedly ischaemic myocardium. In 12 patients with coronary one-vessel disease and without previous transmural myocardial infarction, elective coronary angioplasty (PTCA) was performed (balloon inflation for 2 min). After elective PTCA of the LAD, a significant rise in the proportion of activated neutrophils was noted. After elective 2 min PTCA of the LAD, coronary sinus blood samples showed a marked rise of FMLC stimulated superoxide anion production, whereas passive deformability decreased considerably. Furthermore, an increase in chemotactic activity in coronary sinus blood samples was observed.

The discovery of new properties of angiotensin converting enzyme (ACE) inhibitors in addition to their well-known ability to lower blood-pressure, such as antiproliferative actions and antiadrenergic and vagal-stimulating effects, has contributed to the usefulness of this class of agents in the prevention and treatment of cardiovascular diseases.The contribution of an activated endocrine and/or cardiac paracrine renin-angiotensin system to the progression of cardiovascular diseases with the exception of renovascular hypertension is not fully understood. In particular, the following questions were addressed: 1) Is the facilitation of noradrenaline release in the genesis of arrhythmias a target for ACE inhibition? 2) Is an impaired nutritional cardiac blood flow in heart failure a target for ACE inhibition? 3) Is the intimal hyperplasia that results from coronary angioplasty a target for ACE inhibition? 4) Is the diastolic dysfunction associated with left ventricular hypertrophy in essential hypertension a target for ACE inhibition? In an isolated rat heart preparation with ischemia-induced arrhythmias, none of the ACE inhibitors nor an angiotensin II antagonist was able to significantly suppress the incidence or severity of arrhythmias. In 12 patients with New York Heart Association functional class II-IV heart failure, a fall in cardiac filing pressures after ACE inhibition was associated with an immediate rise in cardiac output and an increase in coronary blood flow of almost 30%. In 24 patients with angina at rest, a preceding percutaneous transluminal coronary angioplasty, and a second angioplasty, control angiograms at 6 months revealed a high degree of restenosis in both ACE inhibitor-treated and placebo patients. Luminal narrowing amounted to 72% in the placebo group and 61% in the ACE inhibitor group. The differences between placebo and enalapril were statistically not significant. In 12 patients with essential hypertension treated with 5 mg cilazapril, left ventricular mass was reduced by 30%, which was closely related to the change in mean arterial blood pressure. The concomitant normalization of the diastolic filling pattern by ACE inhibition, however, was not related to the respective changes in blood pressure.Promising experimental data regarding the antiproliferative effects of ACE inhibitors in preventing restenosis could not be transferred into clinical benefits for patients who underwent repeat coronary angioplasty. Possible antiarrhythmic effects of ACE inhibitors are not likely to be caused by their suppression of noradrenaline release during myocardial ischemia. ACE inhibition was effective in reducing coronary resistance in patients with severe heart failure, thereby augmenting nutritional cardiac blood flow. ACE inhibition also effectively induced a regression of left ventricular hypertrophy in essential hypertension. The associated normalization of diastolic filling pattern may represent an important goal in the treatment of hypertension.

Recent studies have improved our understanding of the beneficial actions of calcium antagonists on myocardial microcirculation and metabolism. The effect of calcium antagonists on the microcirculation of the left ventricular rat myocardium was studied using in vivo microscopic techniques. Intravenous verapamil 0.3 mg/kg and nifedipine 75 micrograms/kg produced a 15 to 18% increase in the diameter of larger A1 and A2 coronary arterioles (range 31 to 300 microns); diameters of terminal (A4) arterioles and capillaries did not change significantly. Furthermore, verapamil significantly (p less than 0.001) increased the ratio of capillaries filled with red cells to those containing plasma alone. Verapamil pretreatment produced a similarly selective dilatation of larger coronary arterioles and protected against the ischaemia-induced fall in capillary red cell content. Spectroscopic data show that verapamil also produces an increase in myocardial phosphocreatine and preservation of adenosine triphosphate (ATP) during ischaemia in the Langendorff-perfused heart. In patients with exercise-induced angina, gallopamil decreased global myocardial 201Tl and 123I phenylpentadecanoic acid (IPPA) uptake due to a reduction in myocardial oxygen consumption. Regional 201Tl and IPPA uptake as well as IPPA clearance in post-stenotic areas tended to rise after gallopamil treatment. Thus, the beneficial effects of calcium antagonists such as verapamil or gallopamil in patients with ischaemic heart disease may result from dilatation of predominantly larger arterioles. Consequently, there is an improvement in regional perfusion and free fatty acid utilisation in reversibly ischaemic regions.

Summary: The aim of this study was to assess the behavior of the diastolic left ventricular (LV) filling pattern and cardiac hypertrophy after treatment with cilazapril. Twelve patients (9 male and 3 female) with mild to moderate essential hypertension, aged 46 ± 14.1 years, were treated with cilazapril for 1 year. They underwent Doppler echocardiography at the beginning (I), after 6 months (II), and after 1 year (III) of treatment. The following parameters were evaluated: mean arterial pressure (MAP) automatically recorded for 24 h, interventricular septal and posterior wall thickness, LV and end-diastolic diameter, LV mass index, early (E) and late (A) diastolic filling flow velocities, and the ratio E/A. A significant reduction in LV hypertrophy and an improved diastolic filling pattern of the left ventricle was shown after 6 months of therapy with cilazapril; this improvement still remained after 1 year of therapy.

This study investigated local alterations in neutrophil activation and deformability after intermittent claudication. In 17 patients with one-sided peripheral arterial occlusive disease, neutrophil count, proportion of activated neutrophils (by nitro blue tetrazolium test), and neutrophil filterability as a measure of passive deformability were assessed in the femoral arterial and venous blood of the diseased leg and in the femoral venous blood of the healthy leg (n = 10). The values were obtained at rest, immediately after claudication, and 10 minutes after claudication induced by repetitive toe stands. Immediately after exercise, the arterial and venous blood differences in the diseased leg were 1) neutrophil count, 9% (95% confidence interval [CI], 5-14%; relative increase in the venous blood compared with arterial blood); 2) the proportion of activated neutrophils, 26% (CI, 10-42%); and 3) the neutrophil filterability, -10% (CI, -4% to -15%). At rest and 10 minutes after exercise, neutrophil parameters did not differ significantly between the femoral arterial and venous blood. Furthermore, no arterial and venous blood differences in the neutrophil parameters were found in the healthy leg. In addition to local changes, systemic changes occurred immediately after exercise. In the femoral arterial blood, the total neutrophil count had risen by 13% (CI, 8-18%), the proportion of activated neutrophils had risen by 41% (CI, 25-58%), and average neutrophil rigidity had risen 17% (CI, 11-22%) compared with the values obtained before exercise. At 10 minutes after exercise, all neutrophil parameters were still elevated. We conclude that even short periods of ischemia, as in intermittent claudication, cause local alterations in neutrophil function and distribution.

To gain further insight into the mechanism of angina in patients with normal coronary angiograms (Syndrome X), a standard exercise test was performed and coronary blood flow and myocardial lactate metabolism were assessed at rest and during dipyridamole-induced vasodilation in 32 patients with this syndrome. In 25 out of these 32 patients, the response of pulmonary artery pressure and left ventricular ejection fraction to dynamic exercise was determined. Results were compared with those obtained in 30 patients without detectable heart disease. Patients with Syndrome X had a positive exercise test, minimal coronary resistance was twice as high as in controls, and significant lactate production occurred upon infusion of dipyridamole. At similar workload, pulmonary artery pressure was significantly higher in patients with typical angina than in controls, and left ventricular ejection fraction did not increase, in contrast to control patients, who showed an increase in left ventricular ejection fraction of more than 5% in response to exercise. These results indicate that symptoms in patients with Syndrome X are due to myocardial ischemia, which may precipitate left ventricular dysfunction during exercise.

The severity of heart failure is in general expressed either by a grading system or by indices of left ventricular function. However, the correlations between currently used classification systems of heart failure and prognosis are poor, and more important, this stratification does not provide a basis for individually adjusted therapy. Treatment of the cause of heart failure is possible, for example, in cases of valvular heart disease. It is not possible when myocardial pump failure is present — except by complete exchange of the diseased heart.

Haemophilus aphrophilus was isolated from 5 blood cultures of a 31-year-old male patient who developed septicaemia two years after heart surgery. The bacteriological and clinical properties of H. aphrophilus are discussed in view of the available literature.

The effects of exogenous and endogenous adenosine on exocytotic noradrenaline release were studied in rat hearts perfused in situ. Exocytotic release of endogenous noradrenaline (determined by high pressure liquid chromatography) was induced by electrical stimulation of the left cervicothoracic ganglion. Exogenous adenosine significantly reduced noradrenaline overflow from the heart. This suppression of noradrenaline overflow was not influenced by desipramine, indicating a mechanism independent from noradrenaline reuptake. The A1 subtype specific agonists cyclohexyladenosine and R-phenylisopropyladenosine had inhibitory effects at lower concentrations than adenosine and S-phenylisopropyladenosine, suggesting the relevance of presynaptic inhibitory adenosine receptors of the A1 subtype. Short ischemic periods of 3 minutes resulted in a marked coronary venous overflow of adenosine during reperfusion. This was accompanied by an inhibition of noradrenaline release evoked by nerve stimulation during ischemia. The adenosine antagonists theophylline and 8-phenyltheophylline prevented this suppression of noradrenaline release. Blockade of oxidative phosphorylation by cyanide in combination with glucose-free perfusion induced an increased formation of endogenous adenosine and suppression of stimulation-evoked noradrenaline overflow. Again, in the presence of the adenosine antagonists theophylline or 8-phenyltheophylline, this suppression was abolished. These results indicate that adenosine is a potent inhibitor of exocytotic noradrenaline release in the heart with relevance during conditions of increased endogenous adenosine formation such as myocardial ischemia.

The cause of syndrome X, i.e. typical angina, positive exercise test, normal coronary angiogram, normal resting cardiac function, but reduced coronary vasodilator capacity is still unknown. The purpose of the study was to investigate blood fluidity as a possible cause of syndrome X. Haematocrit, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability were examined in 14 patients with syndrome X (group 1), 24 patients with typical angina, positive exercise test, but normal coronary vasodilator capacity (group 2), and 37 patients with atypical chest pain and normal coronary arteries (control group). Coronary vasodilator capacity was determined by the argon method. Compared with normals, patients with syndrome X showed an elevated plasma viscosity (1.31 +/- 0.05 mPas vs 1.26 +/- 0.04 mPas, 2P less than 0.01), an elevated erythrocyte photometric aggregation index (141 +/- 27% vs 100 +/- 23%, 2P less than 0.01) and a reduced erythrocyte filterability (0.51 +/- 0.12 vs 0.66 +/- 0.09, 2P less than 0.01). Significant differences in the haemorheologic parameters between group 1, group 2 and the control group, however, were not detected. Multiple regression analysis did not reveal a significant relationship between coronary vasodilator capacity and the haemorheologic parameters tested. The data suggest that the reduction in coronary vasodilator capacity in patients with syndrome X cannot be attributed to haemorheologic alterations.