Calculation of the aortic valve gradient from the left ventricular-femoral and aortic-femoral pairs of pressure waveforms.

Accurate measurement of the transaortic gradient is important in the invasive assessment of the significance of aortic stenosis. The mean gradient obtained from simultaneous left ventricular and aortic pressure recordings is the gold standard, but requires two central catheters. We hypothesized that a gradient calculated by subtracting the aortofemoral from the ventriculofemoral gradient would reproduce the ventriculoaortic gradient. In 24 patients sequential recordings of the aortofemoral, ventriculofemoral, and ventriculoaortic pressures pairs were obtained. The calculated ventriculoaortic gradient was obtained by subtracting the aortofemoral gradient from the ventriculofemoral gradient. Both of these gradients were measured by computer, using a systolic ejection period between the crossovers of the upslope and downslope of the left ventricular waveform with the femoral waveform. The ventriculoaortic gradient calculated using this technique correlated closely with the gradient measured by two central catheters (R = 0.99). This technique is accurate and does not require two central catheters.

Acquired left ventricular to right atrial intracardiac shunt after myocardial infarction: a case report and review of the literature.

A patient without a history of heart disease was seen in our institution after 3-week history of progressive weakness, dyspnea, and orthopnea. Transthoracic echocardiography demonstrated inferoposterobasal akinesis and a left ventricular to right atrial shunt through the coronary sinus, which was confirmed on cardiac catheterization. This is only the second case reported in the English-language literature documenting this rare shunt after a myocardial infarction.

The relationship of anticoagulation level and complications after successful percutaneous transluminal coronary angioplasty.

The degree of anticoagulation and its effect on the frequency of abrupt coronary artery closure, coronary ischemia, bleeding complications requiring transfusion, and death were examined in 336 patients after elective percutaneous transluminal coronary angioplasty (PTCA). All patients received a bolus of 10,000 U of heparin at the beginning of the procedure followed by a continuous infusion of 2000 U/hr. At the conclusion of the procedure the infusion was reduced to 1000 U/hr and continued for 18 to 24 hours at which time the heparin infusion was suspended to allow removal of arterial and venous access sheaths. Partial thromboplastin time (PTT) was examined while patients continued to receive the heparin infusion. There was a variable degree of PTT prolongation in response to a standard dose of heparin with a range of 34 seconds to "greater than 150 seconds." Patients were divided into two groups according to the degree of heparin-induced PTT prolongation: group A included 271 patients with PTT greater than or equal to 3 times the control value, and group B comprised 65 patients with PTT less than 3 times the control value. Ischemic complications were analyzed on day 1 after PTCA and at hospital discharge. Bleeding complications and mortality were examined only at hospital discharge. There was a significant reduction in the incidence of abrupt coronary artery closure in group A on day 1 (1.5% vs 10.7%, p less than 0.001) and at hospital discharge (2.6% vs 10.7%, p less than 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatic and renal metabolism before and after portasystemic shunts in patients with cirrhosis.

Hepatic cirrhosis with portal hypertension and gastroesophageal hemorrhage is a disease complex that continues to be treated by surgical portasystemic shunts. Whether or not a reduction or diversion of portal blood flow to the liver adversely affects the ability of the liver to maintain fuel homeostasis via gluconeogenesis, glycogenolysis, and ketogenesis is unknown. 11 patients with biopsy-proven severe hepatic cirrhosis were studied before and after distal splenorenal or mesocaval shunts. Hepatic, portal, and renal blood flow rates and glucose, lactate, pyruvate, glycerol, amino acids, ketone bodies, free fatty acids, and triglyceride arteriovenous concentration differences were determined to calculate net precursor-product exchange rates across the liver, gut, and kidney. The study showed that hepatic contribution of glucose and ketone bodies and the caloric equivalents of these fuels delivered to the blood was not adversely affected by either a distal splenorenal or mesocaval shunt. In addition to these general observations, isolated findings emerged. Mesocaval shunts reversed portal venous blood and functionally converted this venous avenue into hepatic venous blood. The ability of the kidney to make a substantial net contribution of ketone bodies to the blood was also observed.

Hepatic, gut, and renal substrate flux rates in patients with hepatic cirrhosis.

The roles of liver, kidney, and gut in maintaining fuel homeostasis were studied in 28 patients with severe hepatic cirrhosis, 25 of whom had alcohol-induced cirrhosis. Hepatic, portal, and renal blood flow rates were measured and combined with substrate concentration differences across liver, gut, and kidney to calculate the net flux of free fatty acids, ketone bodies, triglycerides, and glucose with selected glucose precursors, including glycerol, lactate, pyruvate, and amino acids. Data from the catheterization studies were related to hepatic histology, glycogen content, and activities of gluconeogenic enzymes and compared with data obtained from control patients. The effects of food deprivation on net flux of fuels across the liver, gut, and kidney were assessed after overnight and after 3d of fasting. Activities of gluconeogenic enzymes were normal, but hepatic glycogen content was diminished in cirrhotic livers, probably as a consequence of extensive hepatic fibrosis. Extrahepatic splanchnic tissues (gut) had only a small influence on total splanchnic flux rates of carbohydrates, lipids and, amino acids. In cirrhotic patients, there was no mean renal glucose contribution to the bloodstream after an overnight or after a 3-d fast. After an overnight fast hepatic glucose production in patients with cirrhosis was diminished as a result of low-rate glycogenolysis. Hepatic gluconeogenesis and ketogenesis were increased. This pattern of hepatic metabolism mimics that seen in "normal" patients after more advanced stages of starvation. After 3 d of starvation, patients with hepatic cirrhosis have hepatic gluconeogenic and ketogenic profiles comparable to those of normal patients undergoing starvation of similar duration. Nevertheless, the total number of caloric equivalents derived from ketone bodies plus glucose corrected for recycled lactate and pyruvate added to the bloodstream by the cirrhotic livers that could be terminally oxidized by peripheral tissues was less than the contributions made by the normal livers, both after and overnight and after a 3-d fast.

Hepatic metabolism in patients with alcoholic cirrhosis.

Fuel homeostasis was studied in 15 patients with hepatic cirrhosis who previously had sustained upper gastrointestinal hemorrhage secondary to portal hypertension. By combining substrate arteriovenous concentration differences with measured hepatic blood flow rates, the exchange rates of metabolites across the liver was calculated. Hepatic extraction of acetoacetate, beta-hydroxybutyrate, lactate, pyruvate, analine, and glycerol was studied. After an overnight fast, splanchnic glucose production in 15 cirrhotic patients was diminished markedly. Despite reduced total glucose production, there was no decrease in hepatic gluconeogenesis; instead, there was increased glucose formation from amino acids, glycerol, lactate, and pyruvate. In patients with hepatic cirrhosis, the liver does not produce as much glucose as does a normal liver; the failing cirrhotic liver is capable of maintaining fuel homeostasis by increased ketone-body production.

Computer analysis of left ventricular dynamic geometry in man.

Analysis of left ventricular performance in 20 normal patients was undertaken using biplane cineangiography and a semiautomatic computer image processing system. The analysis included evaluation of volumes, ejection fraction, regional shortening, patterns of ejection and filling and, when simultaneous left ventricular pressure was recorded stroke work, stroke power, wall stress and internal myocardial work. All of these data were calculated from digitized images stored permanently on digital magnetic tape, and can be reproduced without reanalysis of the cine film. Normal left ventricular function is described by an end-diastolic volume index of 82 +/- 3 ml, an ejection fraction of 60 +/- 2 percent, left ventricular mass index of 97 +/- 6 g/m2, peak first derivative of volume (dV/dt) of 485 +/- 28 ml/sec, anterior shortening of 48 +/- 2.3 percent, inferior shortening of 33 +/- 1.7 percent, lateral shortening of 29 +/- 1.5 percent, anterior mean shortening velocity (Vcf, in percent of end-diastolic length [L]/sec) of 1.5 +/- 0.1 L/sec, inferior Vcf of 1.1 +/- 0.06 L/sec and lateral Vcf of 0.94 +/- 0.2 L/sec, stroke work of 1.33 +/- 0.21 joules, mean stroke power of 3.7 +/- 0.62 joules/sec, integrated left ventricular pressure (tension-time index) of 2,866 +/- 340 mm Hg-sec, and integrated stress (stress-time index) of 7,260 +/- 765 (X 10(3)) dynes sec/cm2. Internal myocardial work was calculated from the strain energy. More internal work was expended in circumferential than logitudinal shortening (circumferential, 0.69 +/- 0.1 joules; longitudinal, 0.41 +/- 0.08, P less than 0.01), because hoop stress was greater than meridian stress (hoop, 201 +/- 20 dynes/cm3 X 10(3); meridian, 126 +/- 13, P less than 0.001). This analysis of left ventricular performance provides a reliable means for identifying abnormal ventricular function and may be more sensitive than any one measurement alone. The use of digital image processing makes this complex functional analysis of left ventricular performance feasible.

Coronary neovascularity and fistula formation: a sign of mural thrombus.

Fifteen patients have shown neovascularity in the left heart during selective coronary arteriography, with associated fistulous communication to a cardiac chamber in ten. In nine the abnormalities were adjacent to and within ventricular mural thrombi, associated with ventricular aneurysms in seven and congestive cardiomyopathy in two. In six patients with mitral stenosis and atrial fibrillation the angiographic changes related to left atrial thrombi. Histologic study of two atrial thrombi showed revascularization patterns in keeping both with the angiographic findings and with an intermediate stage in the evolution of mural thrombus. Though myxomas can produce a similar appearance, clinical and additional angiographic features should permit differentiation in most instances between this infrequent tumor and the far more common mural thrombus.

Human splanchnic metabolism during diabetic ketoacidosis.

Splanchnic exchange rates of glucose, acetoacetate, beta-hydroxybutyrate, lactate, pyruvate, glycerol, alanine, glutamine, glutamate, free fatty acids, and triglycerides were measured in eight patients during moderate to severe diabetic ketoacidosis. Their arterial glucose concentration was 20.68 (9.80-52.79) mumole/liter and tic glucose release was 0.77 (0.09-2.44) mmole/min. Gluconeogenesis accounted for about one-half of net splanchnic glucose release, assuming quantitative conversion of net splanchnic extracted lactate, pyruvate, glycerol, alanine, and alpha-ketoglutarate equivalents to glucose. Net splanchnic free fatty acid extraction was 0.24 (0.09-0.52) mmole/min. There was a positive correlation between free fatty acid uptake and ketone-body release. Net splanchnic acetoacetate release was 0.50 (0.05-0.92) mmole/min and beta-hydroxybutyrate release was 0.35 (-0.16 to 0.84) mmole/min. Total ketone-body release was 0.84 (0.37-1.61) mmole/min. The wide ranges of net splanchnic glucose and ketone-body production rates show the heterogeneous characteristics of the diabetic patient in ketoacidosis. It is concluded that the hyperglycemia and hyperketonemia of diabetic ketoacidosis is due to the lack of reciprocity among rates of hepatic glycogenlysis, gluconeogenesis, and ketogenesis resulting in inappropriate net splanchnic release of glucose and ketone bodies.

A heart model for understanding three-deminsional cardiac anatomy.

A simple procedure for making cardiac casts has been described. These casts aid in the understainging of the special relationships of the ventricles, valves and coronary arteries as they appear at the time of cardiac angiography.

Cardiac volume measurement errors.

Measurements of cardiac volumes based on biplane radiographic data exhibit a cyclical variation as the heart is rotated with respect to the radiologic instrumentation. This study develops a theoretical basis for evaluating the measurement errors due to orientation, that explains the cyclical variation. Since this type of measurement error is always one of overestimation, better accuracy will be obtained if several views are performed at varying orientations and the smallest of the resulting values is used as the measurement.

Systemic arteriovenous fistula simulating severe valvular aortic stenosis.

A patient with a renal arteriovenous fistula is described. She was though to have valvular aortic stenosis because of a history of rheumatic fever, symptoms of congestive heart failure and syncope, and the presence of a harsh systolic murmur with a thrill in the aortic area. Cardiac catheterization revealed a left-to-right shunt of 8.7 L/min. Ligation of the fistula resulted in complete relief of the symptoms and attenuation of the murmur.

Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence of absence of asynergy.

The relation of minor and major axes of the left ventricle was determined in 100 left ventriculograms performed in the right anterior oblique projection. This relation taken over a wide range of volumes was used to derive a theoretically correct equation for determination of ventricular volume by echocardiography. The final equation was: V =[7.0/2.4 +d] (D3), where V = volume and D = the echocardiographically measured internal dimension. In 12 patients without asynergy, this equation accurately and directly calculated end-systolic and end-diastolic volumes whether the left ventricle was small or large. However, in 12 patients exhibiting left ventricular asynergy the correlation between angiographically and echocardiographically determined volumes was poor. Thus, caution is recommended in the use of time-motion echocardiography to calculate ventricular volumes in patients with coronary artery disease and possible left ventricular asynergy.

Pseudomalfunction of a Beall mitral valve prosthesis in the presence of paravalvular aortic regurgitation.

Premature closure of a Beall mitral valve prosthesis is described in a patient with aortic prosthetic paravalvular regurgitation. Differentiation from valvular malfunction and diagnostic confirmation by means of cinefluoroscopy and simultaneous electrocardiography are discussed.

The evaluation of left ventricular function in man. A comparison of methods.

Comparisons of the sensitivities of parameters for assessing left ventricular performance in man were made in 38 patients. The parameters compared were the ejection fraction, ventriculographic contraction patterns, the left ventricular end-diastolic pressure, and the contractile indices including the contractile element velocity at 10 mm Hg (Vce 10) and maximal contractile element velocity (Vmax). The contractile indices were obtained by catheter tip manometry, utilizing developed pressure (DP) to calculate the velocity of contractile element shortening (Vce) from the formula: dp/dt divided by 32 DP. Vce 10 was measured directly and Vmax was derived by linear manual extrapolation of the pressure-velocity plot to 0 mm Hg. Vmax values derived from linear manual extrapolation were compared with values obtained by computer least squares fitting of the Vce and developed pressure data points to single and double exponential equations. The Vce and developed pressure data points fit the single exponential equation better than the double exponential equation but the use of either equation resulted in slightly higher values for Vmax than obtained with linear manual extrapolation. The effect of heart rate on myocardial contractility was eliminated by making comparisons at both a basal and atrial paced rate of 100. Utilizing all methods, 24 patients were identified to have ventricular dysfunction. The contractile indices were significantly less sensitive than any other parameter (P smaller than 0.05) and identified seven patients while the left ventricular end-diastolic pressure, ejection fraction, and presence of asynergy identified 15, 15, and 12 patients, respectively. The use of a common atrial paced rate of 100 did not increase the sensitivity of the contractile indices. Since there was only partial overlapping between parameters in the identification of left ventricular dysfunction, the combination of different parameters was more sensitive than any single parameter alone. It is concluded that several methods are required to identify all patients with left ventricular dysfunction and that the contractile indices are the least sensitive indicator of left ventricular dysfunction.