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Simultaneous measurements of the concentration of dye by a fiberoptic catheter and of the temperature by a thermistor catheter were obtained in dogs. No significant difference for cardiac output and stroke volume was found. The slightly but significant higher residual fraction by thermodilution than by fiberoptic technique is caused by cold transfer between ventricular myocardium and cavity. It becomes evident after the fifth beat.

In a prospective, randomized and controlled study, 29 patients received i.v. verapamil, 5-10 mg/h for two days, at a mean of eight hours after onset of myocardial infarction. In a control group, 25 patients received no specific treatment. In all patients, left ventricular end-diastolic pressure was initially less than 15 mm Hg. The two groups were comparable as to age, infarct site and haemodynamics (measured via Swan-Ganz catheter). CK and CKMB peaks were significantly lower in the verapamil than the control group (CK 547 vs 703 U/1, P less than 0.05; CKMB 51 vs 68 U/1, P less than 0.025), as well as infarct weight (CK = 48 vs 65 g-equivalent; P less than 0.03; CKMB = 31 vs 49 g-equivalent; P less than 0.005). Arterial blood pressure was lower by 10 mm Hg than in the control group. Peripheral resistance and filling pressure remained unchanged. In patients without left ventricular failure verapamil reduces the infarct size by about 30%. The most prominent haemodynamic change is a reduction in blood pressure.

The effect of captopril on infarct size and arrhythmias was determined in a prospective, randomized, placebo-controlled double-blind study of 46 patients (9 women, 37 men; mean age 61 [38-86] years). Within 2-18 hours of entry into the study these patients received either a slow intravenous bolus injection of 2.5 or 5.0 mg captopril followed by a continuous infusion of 1.5-2.0 mg/h for a period of 48 hours (n = 22), or of a placebo by the same mode of administration (n = 24). The two groups were comparable as to age, infarct site and time of intervention. All patients, except one in each group, also received nitroglycerin (1.2-6.0 mg/h intravenously). QRS complexes were measured to provide a necrosis index. Q-wave amplitudes decreased under captopril (-0.08 +/- 0.04 mV) while increasing under placebo (+0.15 +/- 0.04 mV; P less than 0.05). The number of ventricular extrasystoles in the first 24 hours after onset of treatment or on placebo was 25/h and 9/h, respectively (P less than 0.02). Ventricular fibrillation occurred in 7 patients of the placebo group, in none of the captopril group. Creatine-kinase infarct weight was 59 and 45 gram-equivalents, respectively (placebo vs treated group: not significant). The mean arterial blood pressure fell by 14 mm Hg during the first hour in the captopril group, but by only 3 mm Hg on placebo (P less than 0.01). These results indicate that captopril has a favourable influence on infarct size and electrical stability which is additional to that provided by standard nitroglycerin treatment.

HISTORY AND CLINICAL FINDINGS A 31-year-old woman with known postrheumatic mitral valve stenosis developed for the first time left heart failure in the 19th week of her fifth pregnancy. After intensive drug treatment she was in stage 3 (New York Heart Association classification). Apart from that the patient was in a good general condition and obstetrical status was according to the estimated duration of pregnancy. Auscultation revealed an apical diastolic murmur and mitral opening snap. INVESTIGATIONS Echocardiography demonstrated a mitral valve opening area of 0.85 cm2 (pressure-half time method); the mean gradient was 19 mm Hg. TREATMENT AND COURSE Because of the severity of the findings a percutaneous transvenous balloon valvotomy (according to Inoue) was performed in the 27th week of pregnancy, after careful lead shielding of abdomen and pelvis. Radiological screening time was 10 min. The invasively measured transvalvar pressure gradient was reduced from 28 to 4 mm Hg, echocardiographically determined mitral opening area increased to 1.5 cm2. Delivery was induced in the 36th week of pregnancy because of third-degree renal pelvis congestion. A healthy child, weighing 2850 g was delivered vaginally. CONCLUSION High-grade symptomatic mitral stenosis can, if necessary, be treated with a low-risk to mother and child by percutaneous balloon valvotomy.

To test whether angiotensin-converting-enzyme (ACE) inhibitor can counteract nitrate tolerance, 15 men (mean age 65 [55-69] years) were studied. They all had an at least 75% stenosis of a main coronary artery branch, proven by coronary angiography no longer than 6 months previously. Each patient underwent six ergometric tests (two each per day on alternate days) at constant exercise level and duration: the sum of S-T segment depressions was measured during the recovery and exercise minutes. The initial ergometry test was done without medication, when the S-T segment sum was 1.15 +/- 0.20 mV. After 25 mg captopril (2nd ergometry period) this sum fell to 0.80 +/- 0.18 mV. Two hours after application of a nitrate plaster the S-T segment sum was 0.55 +/- 0.12 mV (3rd ergometry period). Adding 25 mg captopril a further reduction to 0.35 +/- 0.10 was achieved (4th ergometry period). Subsequently, continuous nitrate application brought about nitrate tolerance. The 5th ergometry period then produced a sum of S-T segment depressions of 0.85 +/- 0.18 mV. Renewed captopril administration reduced this value to 0.50 +/- 0.13 mV (57% of the initial value). The effect of captopril in nitrate tolerance is apparently due to an addition of the anti-ischaemic action of the ACE inhibitor (31%) and the residual effect of the nitrate (26%).

It is known from experiments that angiotensin converting enzyme (ACE) inhibitors can limit infarct size. We examined the effect in patients.In a prospective, randomized, placebo-controlled double blind study, 22 patients were given 1.5-2.0 mg captopril/h i.v., while 24 patients were given placebo. Medication was started between 2 hours and 18 hours from the onset of infarction. The two groups were matched for age, infarct location, and time of intervention. With exception of one patient in either group, all were concurrently given nitroglycerin. The necrosis parameters were provided by the quantitative measurement of the QRS complex.The Q wave decreased with captopril treatment (-0.003 mV), but increased with placebo (+0.14 mV) (p0.05). The number of ventricular premature beats at 24 hours from the start of treatment was 25/h with placebo, and 9/h with captopril (p0.02). Ventricular fibrillation occurred 7 times in the placebo group, but did not occur in the captopril group. The creatine kinase (CK) infarct weight was 59 gram-equivalents (gEq) with placebo, and 45 gEq with captopril (p = NS). The mean arterial pressure was reduced by 12 mmHg with captopril treatment.The results show a beneficial effect of captopril on infarct size and electrical instability, over and above the effect of standard management with nitroglycerin and thrombolysis.

A new angiographic method of determining the anatomy of a patent ductus arteriosus (PDA) preparatory to its surgical or nonsurgical closure has been developed and compared to conventional angiographic techniques in 17 patients using a new low pressure balloon catheter (Edwards). The balloon, 5 cm long, is filled with contrast material and expanded to any diameter up to 20 mm. It may be passed into the ductus from either the arterial (14 patients) or venous (3 patients) side. The balloon is expanded by radiopaque material adjacent to the aortic orifice of the PDA and advanced (or pulled) through the ductus. Deformation of the balloon identified the lenght and caliber of the PDA providing virtually identical estimates there of in all 17 patients when compared to conventional angiography. On the other hand, visualization of the PDA was good in only 41 (62%) or tolerable in 14 (21%) of 66 conventionally studied patients. (J Interven Cardiol 1988: 1:2)

Intra-venticular pressures were measured at rest and during simulated exercise before and after intravenous administration of 0.6 mg beta-methyldigoxin in 16 patients (right ventricular measurements in 11, left ones in five), measurements in the right ventricle being taken before and 30-45 min after, in the left ventricle before and 20 min after injection of the drug. There was an increase in stroke volume and maximal cardiac work, while end-diastolic pressure fell. Cardiac glycosides can, therefore, favourably influence congestive cardiac failure on physical exertion. Digitalization indicated in those patients who, on exercise, have an increased end-diastolic pressure and reduced contractility. The positive digitalis effect consists of improved contractility and sustained reduction in end-diastolic pressure. On maintenance digitalization it is to be expected that the heart will profit from both mechanisms, both at rest and during exercise. The increased contractility caused by the glycosides is, however, so small that it does not cause any significant change in oxygen consumption.

In 38 patients with acute myocardial infarction the effect of nitroglycerin on infarct size was studied. Patients were randomized into two groups. 16 patients received continuous nitroglycerin infusions of 0.6 to 6.0 mg/h (mean 2.3 mg/h) over a 48 h period, 22 patients received no specific therapy and served as control. Nitroglycerin was given in the mean 12 +/- 5 (+/- 1 SD) hours following onset of chest pain and 8 +/- 5 after the increase of CK values. Infarct size was determined according to the time activity curve of creatine kinase (CK) and of its myocardial isoenzyme (CK-MB). In all but one patient hemodynamic parameters (left ventricular filling pressure, blood pressure, cardiac index) were measured. The mean infarct size was 51 +/- 30 CK-g-equiv. in control patients, and 48 +/- 33 g in nitroglycerin treated patients. Infarct size as calculated from CK-MB values was 60 +/- 36 g (n=16) in control, and 52 +/- 41 g (n=11) in treated patients. At left ventricular filling pressure values (LVFP) below 20mm Hg infarct size amounted to 43 +/- 30 g (n=12) in control, and to 41 +/- 32 g (n=11) in the nitroglycerin group. At LVFP values above 20 mmHg infarct size was 61 +/- 29 g (n=10) in control as opposed to 64 +/- 32 g (n=5) in treated patients. There was no difference between infarct size as predicted during the first 7 h and the observed infarct size. - Despite the known beneficial effect of nitroglycerin on hemodynamics and on myocardial ischemia, infarct size seems not to be greatly reduced, however, intervention occurred fairly late (12 h). In early intervention beneficfial effects seem likely.

Hemodynamic measurements were obtained for 48 h in 46 patients with recent myocardial infarction. Patients were randomized to treatment with (n = 22) and without nitroglycerin (NTG) n = 24). In patients with diastolic pulmonary arterial pressure (PAEDP) less than 20 mmHg (group I), NTG decreased PAEDP from 15 to 11 mmHg (n = 13); in the untreated control group PAEDP remained unchanged (n = 15). Cardiac output decreased in the NTG group from 5.4 to 5.0 1/min and in the control group from 4.7 to 4.4 1/min. Mean arterial pressure decreased in both groups, in the NTG group from 106 to 97 mmHg and in the control group from 102 to 94 mmHg. In patients with left ventricular failure and PAEDP greater than 20 mmHg (group II) the decrease in left ventricular filling pressure was significantly greater (25 to 17 mmHg, n = 9) than in the control group (24 to 20 mmHg, n = 9). Cardiac output increased during NTG treatment from 4.2 to 5.1 1/min. In the control group, however, cardiac output decreased from 4.2 to 3.6 1/min. Mean arterial pressure decreased from 103 to 95 mmHg in the NTG group and from 114 to 96 mmHg in the control group. Heart rate did not change significantly. Thus, PAEDP decreased significantly in patients who received NTG treatment for 48 h compared to an untreated control group. Cardiac output increased in treated patients, especially those with left ventricular failure, but decreased in the control group. Mean arterial pressure decreased to the same degree in treated patients and in controls.

The effect of nitroglycerin (N.G.) on the size of myocardial infarction was studied in 12 open-chest dogs with chloralose-urethane anesthesia by means of epicardial ECG-mapping and compared with the influence of simple ligature of the same coronary artery branch. In order to identify the specific effect of N.G. on the heart and the coronary circulation without contribution of the peripheral circulation in 6 dogs aortic pressure was stabilized by a clamp placed around the descending aorta and heart rate was kept constant by atrial pacing.

ZusammenfassungUm dem Problem der Anpassung der densitometrischen Meßfelder an jede beliebige Herz- und Gefäßkonfiguration im Röntgenfernsehbild gerecht zu werden, wurde ein System entwickelt, mit dem elektronische Meßareale jeder beliebigen Form und Größe herstellbar sind. Die meisten bisherigen Verfahren verwenden rechteckige Fenster. Grundlage des Systems ist eine Farbfernsehdisplayeinheit zur Einblendung von Daten und Kurven im angiographischen Bild. Mit Kurvenspeicher auf Schieberegisterbasis und einem Lichtgriffel werden bei Bestimmung der Regurgitation in einem ersten Schritt zunächst die Volumina des linken Vorhofes und der linken Kammer videometrisch mehrfach innerhalb einer Periodendauer bestimmt. Nach Errechnung der Volumina sind weiterhin die im Speichermedium eines Rechners archivierten Konturen verfügbar. Zur densitometrischen Messung läßt sich nun mit einem Video-Plattenspeicher der Konturenablauf am Bildschirm wiederholen und auch den folgenden R-R -Intervallen einer biplanen Videoszene wieder überlagern. Die Synchronisation zwischen der im Rechner gespeicherten Konturdynamik und der Röntgenszene erfolgt bei starrer Herzfrequenz mit der R-Zacke und dem Bildzähler. Es ergibt sich somit eine densitometrische Regurgitationsmessung bezogen auf das Volumen des jeweiligen Herzabschnittes.

Circulatory hemodynamics, coronary blood flow and myocardial oxygen consumption were studied in 10 open chest dogs in chloralose-urethan anesthesia during intraaortic balloon-pulsation (IABP).

Nitroglycerin (NTG) hat gunstige Effekte auf die Hamodynamik und myokardiale Ischamie (ST-Hebung) beim frischen Herzinfarkt. Es ist jedoch unklar, ob NTG auch die Infarktgrose selbst beeinflust. 38 Patienten (P) wurden randomisiert: 16 P erhielten NTG uber 2 Tage, 22 P keine spezifische Therapie (Kontrollgr. (K)). Mit NTG wurde im Mittel 12 h nach Auftreten der Symptome begonnen. Die Infarktgrose war in beiden Gruppen gleich (NTG 48 ± 33, K 51 ± 30 g-equiv.). Dieses Ergebnis wurde durch Berechnung der CKMB-Infarktgrose bei 27 der 38 P bestatigt (NTG 52 ± 41, K 60 ± 36 g-equiv.). Zwischen der (aus den ersten 7 h) vorausgeschatzten und der gemessenen Infarktgrose ergaben sich ebenfalls keine Unterschiede. Auch nach Unterteilung der P mit und ohne Linksinsuffizienz (LVEDP 20 mm Hg) waren die Infarktgewichte in der NTG- und K-Gruppe nicht voneinander verschieden. Der systolische und diastolische Pulmonalisdruck und der systemische Widerstand nahmen gegenuber der K-Gruppe ab. — Daraus folgt, das NTG keinen groseren Effekt auf die Infarktgrose hat, wenn auch Hamodynamik und myokardiale Ischamie gunstig beeinflust werden.

Die Bestimmung der Kontraktilitat in Ruhe hat keine wesentliche Bedeutung fur die Unterscheidung von Patientengruppen mit normaler und eingeschrankter Ventrikelfunktion. Deshalb scheint die Eingruppierung des individuellen Patienten nur dann moglich zu sein, wenn der linke Ventrikel einem Stres ausgesetzt wird.

First described in the last century, HOCM is recognized today in a considerable number of patients. The severity of the disorder varies between severe disablement to a completely asymptomatic clinical picture.

Twenty-two patients with hypertrophic obstructive cardiomyopathy were treated with the calcium inhibitor, verapamil, which was administered in a mean oral dose of 480 mg per day. After an average of 15 months of treatment (4 to 24 months), the QRS amplitude in the electrocardiogram was significantly reduced from 4.2 to 3.8 mV. Heart volume calculated from chest x-ray films in the supine position decreased significantly from 858 to 766 ml per 1.73 m2. In 10 patients, follow-up heart catheterisation showed a decrease in left ventricular muscle mass in 7 patients and a slight increase in 3 patients. Coronary artery diameter decreased in 7 patients, increased in 1, and was unchanged in 2. The reduction in coronary artery diameter is considered to be a consequence of a reduced heart muscle mass. From all available clinical data it is concluded that verapamil treatment is superior to beta-blocker therapy.

Seit den Untersuchungen von Bruschke et al. [3,4] ist die Beziehung zwischen Befunden der Koronarographie und Ventrikulographie und der Prognose bei koronarer Herzkrankheit bekannt. Mit zunehmender Koronarsklerose und starkerer Ventrikelschadigung nimmt die Mortalitat deutlich zu [2, 6, 9, 16, 19]. Weit weniger untersucht ist dagegen die Beziehung nichtinvasiver Parameter zur Prognose. In der vorliegenden Untersuchung wurden die quantifizierte Ischamiereaktion im Belastungs-EKG und die radiologisch ermittelte Herzgrose den Befunden der Koronarographie und Ventrikulographie gegenubergestellt und mit der 7-Jahres-Uberlebensrate verglichen [1, 7, 13, 20].

For a comprehensive evaluation of ventricular function, angiographies are required. In this way, the location and the extent of a disturbance of contraction can be seen.

In order to recognize and quantitate abnormalities in wall segment motior in 22 patients simultaneous measurements of isovolumic and ejection phase parameters were performed with the MILLAR-angiographic catheter at rest, after leg raising, and during bicycle exercise. Six patients had slight (stenosis less than 50%) or no coronary heart disease (CHD) (group I), 16 patients had severe CHD (group II, stenosis of more than 50% in 1–3 main branches). During volume load in all patients of group II, a decrease of peak measured velocity (Vpm) and the velocity of circumferential fiber shortening (Vcf from 1.4 to 1.1 circ/sec, p < 0,025) occurred. In group I, Vcf increased (p < 0,05) (Fig. 1).

Die Wirksamkeit der intraaortalen Ballonpulsation im tierexperimentellen kardiogenen Schock wurde wiederholt nachgewiesen (1–3) und hat bei einzelnen klinischen Fallen bereits Erfolge gezeigt (4, 5).

To optimize intraaortic balloon pulsation, the inflation and deflation mechanisms of different intraaortic balloons were studied in a model aorta with pressure volume characteristics approximating those of a natural aorta and in anesthetized dogs by cineangiography. It could be demonstrated that inflation of straight balloons begins at the tip and proceeds from there to the end of the balloon. The distention of the aortic arch balloons is first observed in the aortic arch; inflation than proceeds to the end of the balloon. Deflation of both balloon types has the same direction as inflation, beginning at the tip.From the model investigations it can be concluded that the balloon dynamics are definitely pressure dependent: inflation begins in that balloon part, where the pressure is lowest; deflation where the highest pressure is exerted. These results explain the behavior of balloons in vivo.In the aorta of living dogs in the early diastole, the pressure nearest to the heart is less than in lower parts of t...

The haemodynamic effects of intra-aortic counterpulsation with normally used cylindrical and newly designed aortic arch balloons on the coronary blood flow and the performance of the normal dog heart were compared. Both balloon types resulted in a decrease of left ventricular systolic and end-diastolic pressure, systolic arterial and end-diastolic arterial pressure. The amplitude of diastolic augmentation was significantly larger with the aortic arch balloon. The carotid artery flow increased significantly more with the aortic arch balloon (36%) than with the cylindrical balloon. Pulsation in the aortic arch effected a significant decrease in left ventricular impedance (33%), which was inversely correlated with a marked increment of the stroke volume (36%). In addition, mean coronary blood flow increased during aortic arch balloon pulsation (37%). From these data, it is concluded that optimal intra-aortic balloon pulsation should be performed with large balloons close to the aortic valve. The newly designed aortic arch balloon fulfils this condition.

A visual-display unit, for the simultaneous display of two X ray images together with the results of physiological measurements in the form of digital instantaneous readings and continuous diagrams, with a facility for the keyboarding of patients' names and numbers with comments into the same video field, is demonstrated and discussed with particular reference to its application to the cardiac-catheterisation laboratory.

Der kardiogene Schock entwickelt sich bei Patienten mit akutem Herzinfarkt in etwa 20% (5). Der wesentliche patho-physiologische Mechanismus besteht dabei in einem mechanischen Versagen des Herzens mit Abnahme des Herzminutenvolumens, des arteriellen Druckes und der Koronardurchblutung. Die geringe Erfolgsquote von nur 10–20% bei der medikamentosen Behandlung des kardiogenen Schocks hat die Entwicklung von Pumpsystemen zur Entlastung des Herzens in Gang gebracht. Die intraaortale Ballon-pulsation gehort zu den Gegenpulsationssystemen, die die Druckarbeit des linken Ventrikels durch systolische Druckabsenkung bei gleichzeitiger diastolischer Druckanhebung vermindern (3, 7, 9). Ausgehend von dieser Verbesserung der Haemodynamik der linken Kammer wurden die Auswirkungen der intraaortalen Ballonpulsation im experimentellen kardiogenen Schock beim Hund untersucht.