William Ganz

Catheterization of the Heart in Man with Use of a Flow-Directed Balloon-Tipped Catheter

Abstract Pressures in the right side of the heart and pulmonary capillary wedge can be obtained by cardiac catheterization without the aid of fluoroscopy. A No. 5 Fr double-lumen catheter with a balloon just proximal to the tip is inserted into the right atrium under pressure monitoring. The balloon is then inflated with 0.8 ml of air. The balloon is carried by blood flow through the right side of the heart into the smaller radicles of the pulmonary artery. In this position when the balloon is inflated wedge pressure is obtained. The average time for passage of the catheter from the right atrium to the pulmonary artery was 35 seconds in the first 100 passages. The frequency of premature beats was minimal, and no other arrhythmias occurred.

Measurement of Coronary Sinus Blood Flow by Continuous Thermodilution in Man

A technique was developed for measurement of blood flow in the coronary sinus in man by continuous thermodilution. For single determinations, 5% dextrose at room temperature is injected at a constant rate of 35 ml/min for a period of about 20 sec. In 14 subjects with normal coronary arteries the mean coronary sinus blood flow was 122 ± 25 ml/min (range, 83 to 159 ml/min). The blood flow computed per 100 g of left ventricle was 82 ± 16 ml/min, which is in the range of values obtained by nitrous oxide and coincidence counting methods. In 35 patients with arteriographically confirmed coronary artery disease the mean flow was similar (128 ± 20 ml/min; range, 92 to 167 ml/min).A special catheter was used for simultaneous measurement of blood flow in the coronary sinus and great cardiac vein. In eight normal subjects the mean great cardiac vein flow was 68 ± 11 ml/min (range, 51 to 78 ml/min) or 65 ± 10% of the coronary sinus blood flow. The method allowed continuous measurement of flow over a period of several minutes and, for the first time, measurement of rapid changes in myocardial perfusion.

Early phase acute myocardial infarct size quantification : Validation of the triphenyl tetrazolium chloride tissue enzyme staining technique

Gross histochemical delineation of myocardium which has lost dehydrogenase enzyme activity has been shown to facilitate macroscopic recognition of necrotic myocardium. The present study was undertaken to assess the accuracy of the triphenyl tetrazolium chloride (TTC) technique for quantitating myocardial infarct size very early after coronary occlusion. In 16 closed-chest dogs the left anterior descending coronary artery was occluded with an intra-arterial balloon. Twelve dogs were killed 6 hours after occlusion, their hearts excised, cut from apex to base into 1 cm thick slices, and incubated in TTC. Whole-mount histologic sections of each slice were prepared. Myocardial infarct size was measured by planimetry of photographs of each gross slice and histologic section using classical criteria of necrosis. Myocardial infarct size determined in 54 slices by the TTC technique and histologically was similar (25 +/- 16% vs 27 +/- 16% of the left ventricular mass, mean +/- SD) with close correlation between the two methods (r = 0.91). Four dogs were killed 3 hours after occlusion and TTC stained and unstained myocardium was studied by electron microscopy. When the TTC technique identified necrosis so did electron microscopy. Areas identified by the TTC technique as non-necrotic were either normal or only ischemic by electron microscopy. Thus, using TTC, necrosis can be quantitated reliably 6, and even 3 hours after coronary occlusion, before histologic changes are clearly diagnostic. This technique represents a reliable, practical means for quantitation of recent infarction and for studying the evolution of ischemic injury in its early phase.

A new technique for measurement of cardiac output by thermodilution in man

Abstract A technique for measurement of cardiac output by thermodilution (COTD) in man has been described. Comparison with cardiac outputs determined simultaneously by the dye-dilution technique (CODYE) in 63 measurements in 20 patients showed close agreement of the 2 methods in a range of values from 2.9 to 8.0 liters/min (COTD = 0.96 CODYE + 0.2, r = 0.96). The reproducibility of measurements was 4.1 percent with the thermodilution and 5.4 percent with the dye-dilution technique. The thermodilution technique does not require withdrawal of blood during measurements and removal of blood for calibration. The calibration is simple and accurate. There is virtually no recirculation, so that a simple integrator can be used for determination of the area beneath the thermodilution curve.

Thermodilution cardiac output determination with a single flow-directed catheter.

Abstract A single right heart catheter which allows simultaneous determinations of cardiac output, pulmonary artery pressure, pulmonary capillary wedge pressure, and right atrial pressure in critically ill patients is described. The catheter, which utilizes the thermodilution technique of cardiac output determination, may be rapidly and safely passed at the bedside without fluoroscopy.

Hemodynamic and Metabolic Responses to Vasodilator Therapy in Acute Myocardial Infarction

Hemodynamic effects of vasodilator therapy (phentolamine or nitroprusside) were studied in 38 patients with acute myocardial infarction (AMI). Cardiac metabolism was studied in 19 of the 38 patients. According to the initial level of left ventricular filling pressure (LVFP) and left ventricular stroke work index (SWI), patients were divided into three groups: Group I-nine patients with LVFP 15 mm Hg or less; Group II-14 patients with LVFP > 15 mm Hg and SWI >20 g-m/m2; Group III-15 patients with LVFP > 15 mm Hg and SWI < 20 g-m/ m2. In Group I most patients were clinically uncomplicated. In Group IL most patients had clinical left ventricular failure including one patient who had clinical features of cardiogenic shock. Group III patients all had severe left ventricular failure, with eight patients in clinical shock.In all groups LVFP, pulmonary artery pressure, right atrial pressure, and systemic and pulmonary vascular resistance decreased significantly with vasodilator therapy with only a slight to moderate decrease in arterial pressure. In Group I patients SVI decreased (-7%) together with an increase in heart rate. Significant improvement in left ventricular performance, however, was observed in Groups II and III as indicated by increased stroke volume index (SVI) and cardiac index (CI) and decreased LVFP. The increase in SVI and CI was of similar magnitude in both Group LI (SVI +18%, CI +24%) and Group III (SVI +28%, CI +29%) patients, a change suggesting that vasodilation thereby may be applicable and beneficial even in the presence of severe depression of cardiac performance.Improved left ventricular performance in group II and III patients was accompanied by a slight decrease in coronary blood flow, myocardial oxygen consumption, and transmyocardial oxygen extraction. There was no change in myocardial lactate metabolism in any group. In vitro studies in isolated cat papillary muscle preparations showed no direct positive inotropic effect of either phentolamine or nitroprusside. Thus, significant improvement in left ventricular performance occurs during vasodilator therapy in patients with AMI and elevated LVFP, even in the presence of severe depression of cardiac performance. Furthermore, this improvement is not accompanied by increased metabolic cost. Vasodilator therapy, therefore, may have an important role in the treatment of pump failure complicating myocardial infarction.

Measurement of blood flow by thermodilution

Abstract In thermodilution a known change in heat content of the blood is induced at one point of the circulation and the resultant change in temperature detected at a point downstream. When cardiac output is measured, a bolus of cool liquid is injected into the upper right atrium and the temperature change detected in the pulmonary artery. When flow in single blood vessels is measured, the distance between the site of injection and the site of detection is small; therefore, mixing must be attained by the kinetic energy of the injectate. The continuous constant rate injection technique is most suitable for measurement of venous flow. Since the blood flow in arteries can be markedly and unpredictably altered by the injection or the injectate, this technique is not suitable to measure flow in arteries. Measurement of venous flow by the bolus injection technique is tedious and time-consuming because of the complex formula. Minimal recirculation, simple and accurate calibration, intravascular detection of temperature and simple equipment are the advantages of the thermodilution technique.

Intermittent brief periods of ischemia have a cumulative effect and may cause myocardial necrosis.

We investigated the effects of brief intermittent periods of ischemia on myocardial viability. Brief periodic coronary occlusions were produced up to 18 times by inflating and deflating the balloon of an intracoronary #2F catheter for periods of 15, 10 or 5 minutes, followed by 15‐minuteperiods of reperfusion.Creatine kinase (CK) release, triphenyl tetrazolium chloride staining, and light and electron microscopy were used to detect the presence of myocardial necrosis. For the study of CK release, blood was taken from the great cardiac vein and the aorta before and at 5-minute intervals during each left anterior descending coronary occlusion, as well as during and 1, 5, 10 and 15 minutes after balloon deflation. In seven of 24 dogs with 15-minute occlusions, in five of 21 dogs with 10-minute occlusions, and in three of 32 dogs with 5-minute occlusions, small but distinct areas of subendocardial necrosis were present. In all dogs with morphologic proof of necrosis, there was periodic release of CK into the great cardiac vein, which peaked immediately after reperfusion, reflecting CK washout. Thus, brief periods of ischenia, which when single do not cause necrosis, have a cumulative effect and may cause myocardial necrosis. This mechanism of necrosis may be relevant clinically in patients with frequent anginal episodes. Since many dogs of this study did not have any myocardial necrosis, the findings also suggest that intermittent repefdusion has a beneficial effect and may prevent necrosis, even when total occlusion time exceeds 200 minutes.

Failure of Intracoronary Nitroglycerin to Alleviate Pacing-Induced Angina

Relief of angina by nitroglycerine has been attributed to two possible mechanisms: (1) Increase in myocardial blood supply by direct action of the drug on the coronary arteries. (2) Reduction in myocardial oxygen demand by action of the drug on the systemic circulation. Sublingual application of nitroglycerin in previous studies did not allow the ruling out of the operation of either or both mechanisms. This study was, therefore, designed in such a way that the effect of the direct action of nitroglycerin on the coronary bed on angina could be studied in the absence of changes in the systemic circulation. In 25 patients undergoing cardiac catheterization and coronary arteriography as possible candidates for revascularization surgery, nitroglycerin, 0.075 mg in 1 ml of 5% dextrose, was injected into the left coronary artery through the angiographic catheter during angina pectoris induced by pacing. Coronary sinus blood flow by the continuous thermodilution method, femoral artery blood pressure, and lead V5 were recorded continuously. In 20 patients the procedure was repeated with injection into the right coronary artery. In none of the 25 patients did the intracoronary injection of nitroglycerin alleviate the angina during the 1-min observation period, whether injected into the obstructed artery or into the artery supplying collaterals to the obstructed artery. The intracoronary injection was ineffective despite a significant increase in coronary sinus blood flow in 14, lasting 26 sec on the average. This suggests that the increase in blood flow did not occur in the ischemic areas where it was needed, but in other areas where the arterioles were not maximally dilated by ischemia. This explanation is further supported by the fact that in five patients with very severe restriction of the left coronary artery system the coronary sinus blood flow failed to increase in response to intracoronary nitroglycerin during angina, but increased significantly in response to nitroglycerin after discontinuation of pacing and disappearance of angina. In six patients, 0.2 mg nitroglycerin injected intravenously 1 min following the intracoronary injection relieved the angina unaffected by the preceding intracoronary injection. The relief was associated with a fall in arterial blood pressure and coronary sinus blood flow. The study indicates that the direct action of nitroglycerin on the coronary bed plays little, if any, role in the antianginal effect of the drug, which appears to be due entirely to the action of the drug on the systemic circulation.

ST elevations in leads V1 to V5 may be caused by right coronary artery occlusion and acute right ventricular infarction

In 5 of 69 patients (7%) undergoing intracoronary or intravenous streptokinase treatment, the ST-segment elevations in leads V1 to V5 were caused by occlusion of the right rather than the left anterior descending coronary artery and by myocardial infarction (MI) of the right ventricular (RV) wall rather than the anterior left ventricular (LV) wall or the ventricular septum. RV involvement was documented by technetium pyrophosphate uptake, hypokinesia, dilatation and depressed RV ejection fraction. The left anterior descending artery was patent and the anterior LV wall had normal thallium-201 uptake, no technetium uptake and normal wall motion. ST-segment elevation was highest in lead V1 or V2 and decreased toward lead V5; in patients with anterior LV MI, the ST-segment elevations are usually lowest in lead V1 and increase toward the V5 lead. In contrast to anterior LV infarcts, the R waves in leads V1 to V5 did not decrease and Q waves did not evolve with progression of the MI. The ST-segment elevations in leads V1 to V5 in our patients were associated with small or absent ST-segment elevations in leads, II, III and aVF, suggesting that in other cases of RV infarction, the appearance of ST-segment elevations in leads V1 to V5 is blocked by the dominant electrical forces of the LV inferior MI. This suggestion was confirmed in a canine model. Recognition of the presence of RV infarction may be therapeutically important.