Atrial Pressure Curve Research Articles

P296 HIDDEN PERICARDIAL CONSTRICTION IN A PATIENT WITH CHRONIC PERICARDIAL EFFUSION AND “UNEXPLAINED” DYSPNEA

Abstract Constrictive physiology leads to exertional symptoms related to restrained diastolic filling and intracardiac/intrathoracic dissociation. However, these hemodynamic abnormalities might not be evident in some patients. A 55–year–old woman was referred to our center to perform a right and left cardiac catheterization because of “unexplained” dyspnea. Three years before she was found to have a large idiopathic pericardial effusion. Anti–inflammatory therapy did not result in any improvement. Since then, the patient complained dyspnea NYHA II–III, in the absence of any clinical and imaging sign of tamponade/pericardial constriction. At rest, there was no sign of constriction, but a relative hypovolemic status characterized by low pulmonary and filling pressures and cardiac output (CO) at the lower limits of normal. After a 500 mL saline load and passive legs raising, Kussmaul’s and “M” signs appeared on the right atrial pressure curve (Figure 1), the pulmonary artery wedge pressure (PAWP) – left ventricular end–diastolic pressure (LVEDP) gradient difference between expiration and inspiration was >5 mmHg (Figure 2), and ventricular systolic pressures went out of phase by 180°. Both right and left filling pressures as well as pulmonary pressures steeply increased in a concordant manner by about 10 mmHg after fluid load, in absence of a relevant increase in CO (Figure 3). Physical exercise performed thereafter showed an additional mild increase with a plateau pattern of all pressures, suggesting an upward–shift of the pressure/flow relationship (Figure 3). All these signs suggested a latent constrictive physiology. Despite this, the patient showed an optimal CO reserve coupled with a normal exercise capacity (peak oxygen consumption, VO2, 127% of predicted) that would have argued against our hypothesis. We then performed a diagnostic and evacuative pericardiocentesis. After the drainage of 130 ml of pericardial fluid, LV transmural pressure increased and CO at rest was fully normalized. Moreover, no hemodynamic sign of constriction could be observed even after a 1000 ml saline load. The patient reported disappearance of exertional breathlessness, objectivated by an increase in peakVO2 by 20% as compared with the previous test. Thus, our case underscores how subtle the hemodynamic impact of pericardial effusion can be, with the need of well–tailored diagnostic exams to explain otherwise “unexplained” patients’ symptoms, with potential therapeutic implications.

The Fractured Venous Catheter: Where Is the Remaining Piece?

We present a rare complication concerning a central venous catheter (CVC) during cardiothoracic surgery. An 81-year-old male patient was scheduled for an aortic valve replacement and a MAZE ablation. After induction of general anesthesia and before the start of surgery, a central venous catheter (3 lumen, 7 F, Arrow-Howes, Reading, PA) was placed uneventfully in the right internal jugular vein. The distal lumen (brown) was connected to display the right atrial pressure on the monitor, showing a normal right atrial pressure curve.

Pressure‐Guided Cryoballoon Isolation of the Pulmonary Veins for the Treatment of Paroxysmal Atrial Fibrillation

Pulmonary vein (PV) isolation using a balloon-mounted cryoablation system is a new technology for the percutaneous treatment of atrial fibrillation (AF). Complete PV occlusion during balloon ablation has been shown to predict successful electrical isolation. The aim of this study was to correlate mechanical PV occlusion with changes in a pressure curve recorded at the distal tip of the cryoballoon catheter. We analyzed 51 PVs in 12 patients (61 +/- 6 years old) with paroxysmal AF. At first, PV occlusion via the cryoballoon was documented by changes in the pressure curve. Once the PV is occluded, the pressure curve registered in the vein converts from a left atrial pressure curve to a pulmonary artery pressure curve: the PV wedge curve. Occlusion was then confirmed by transesophageal echocardiography (TEE). Following 2 cryoablation applications, electrical PV isolation was assessed with a circumferential mapping catheter. Under the exclusive guidance of changes in the pressure curve at the tip of the cryoballoon, mechanical occlusion confirmed by TEE was achieved in 47 of 51 PVs (92%). Three PVs required further TEE guidance to achieve occlusion. All 50 occluded veins were electrically isolated after cryoablation. One right inferior vein, which could not be occluded with the balloon, displayed conduction post cryoablation and was isolated by focal ablation. Occlusion and electrical isolation of PVs during cryoballoon ablation can be predicted by the appearance of a PV wedge curve at the tip of the catheter. This new straightforward parameter may facilitate the procedure.

A new cardiopulmonary resuscitation method using only rhythmic abdominal compression: A preliminary report

This article introduces 2 new cardiopulmonary resuscitation (CPR) concepts: (1) the use of only rhythmic abdominal compression (OAC) to produce blood flow during CPR with ventricular fibrillation and (2) a new way of describing coronary perfusion effectiveness, namely, the area between the aortic and right atrial pressure curves, summed over 1 minute, the units being millimeters of mercury per second. We call this unit the coronary perfusion index (CPI). True mean coronary perfusion pressure is CPI/60. We also relate CPI during CPR with ventricular fibrillation to the CPI for the normally beating heart in the same animal, obtained before each experiment. This 11-pig (25-35 kg) study compares the CPI for standard chest-compression CPR and that obtained with OAC-CPR. The coronary perfusion ratio for OAC-CPR compared with standard chest-compression CPR was 1.6 ± 0.73 ( P = .024). In other words, OAC-CPR produced 60% more coronary perfusion than standard chest-compression CPR, with no damage to visceral organs.

Effects of sildenafil on hypoxic pulmonary vascular function in dogs

Sildenafil has been shown to be an effective treatment of pulmonary arterial hypertension and is believed to present with pulmonary selectivity. This study was designed to determine the site of action of sildenafil compared with inhaled nitric oxide (NO) and intravenous sodium nitroprusside (SNP), known as selective and nonselective pulmonary vasodilators, respectively. Inhaled NO (40 ppm), and maximum tolerated doses of intravenous SNP and sildenafil, (5 microg x kg(-1) x min(-1) and 0.1 mg x kg(-1) x h(-1)), respectively, were administered to eight dogs ventilated in hypoxia. Pulmonary vascular resistance (PVR) was evaluated by pulmonary arterial pressure (Ppa) minus left atrial pressure (Pla) vs. flow curves, and partitioned into arterial and venous segments by the occlusion method. Right ventricular hydraulic load was defined by pulmonary arterial characteristic impedance (Zc) and elastance (Ea) calculations. Right ventricular arterial coupling was estimated by the ratio of end-systolic elastance (Ees) to Ea. Decreasing the inspired oxygen fraction from 0.4 to 0.1 increased Ppa - Pla at a standardized flow of 3 l x min(-1) x m(-2) from 6 +/- 1 to 18 +/- 1 mmHg (mean +/- SE). Ppa - Pla was decreased to 9 +/- 1 by inhaled NO, 14 +/- 1 by SNP, and 14 +/- 1 mmHg by sildenafil. The partition of PVR, Zc, Ea, and Ees/Ea was not affected by the three interventions. Inhaled NO did not affect systemic arterial pressure, which was similarly decreased by sildenafil and SNP, from 115 +/- 4 to 101 +/- 4 and 98 +/- 5 mmHg, respectively. We conclude that inhaled NO inhibits hypoxic pulmonary vasoconstriction more effectively than sildenafil or SNP, and sildenafil shows no more selectivity for the pulmonary circulation than SNP.

A Novel Implantable Electromechanical Ventricular Assist Device

A novel ventricular assist device (HIA-EMLVAD-AT1, Helmholtz Institute Aachen-Electromechanical Left Ventricular Assist Device-Animal Test Version 1), driven by a uniformly and unidirectionally rotating actuator and a patented hypocycloidic pusherplate displacement gear unit, was developed and tested in an acute animal experiment. The excellent free filling behavior of the pump chamber with a stroke volume of 65 ml is obtained by a 2:3 ejection-filling time relationship. The uniform motor rotation facilitates simple sensorless pre and afterload detection by motor current analysis. In contrast to common apical cannulation, the inlet cannula was placed via the left atrium through the mitral valve into the left ventricle. This connection mode is preferable for left ventricular recovery and preservation. Left atrial, left ventricular, and aortic pressure curves, as well as pulmonary artery flow data, were obtained. The data show very effective unloading of the natural ventricle and demonstrate the feasibility of this novel assist device. Directions for further improvement of technical features were also identified.

Continuous measurement of intramyocardial pH: Correlation to functional recovery following normothermic and hypothermic global ischemia

The continuaus measurement of imtramyocardial pH was used to follow the progression of ischemia and was correlated to the recovery of left ventricular function following normothermic (38 °C) and hypothermie (25 °C) global ischemia. New miniature myocardial transducers, which incorporate fiberoptic technology and dual pH- and temperature-sensing capability, were placed into the left ventricular free wall and seplum of 52 sheep undergoing cardiopulmonary bypass, Left ventricular stroke work as a functional mean left atrial pressure curves were generated before and after cardiopulmonary bypass by volume loading wilh whole blood. Functional recovery was determined by the ratio of the integrats of the preischemic and postischemic function curves. Control sherp (N = 11) did not undergo ischemia. Three groups (N = 41) or 6.6. The prelschemic myocardial pH averaged 7.42 ± 0.01. Following both normothermic and hypothermic global ischemia, no significant difference was demonstrated in recovery of function between control (pH 7.4) ery of function of the pH 6.8 and pH 6.6 groups was significantly decreased ( p < 0.01) versus cortrol and pH 7.0 groups at both temperatures. No significant difference in recovery of function was demo trated at any pH level when normothermic versus hypothermic groups were cornpared. However, hypothermia provided increased time ( p < 0.001) before each level of function was reached with a slower rate of change of pH ( p < 0.01) compared with the corresponding same pH graup in sheep undergoing normyocardial pH lower than 7.0 at the termination of ischemia resulted in a marked decrease in left ventricular function following both normothermic and hypothermic global recovery at 38 °C and 25 °C, and rate of change of myocardial pH predicted the interval of ischemia required to achieve a give functional level of recovery.

Jugular Venous Pulse in Ebstein's Anomaly: Echocardiographie and Doppler Echocardiographie Study

To clarify the characteristics of the jugular venous pulse and its genesis in Ebstein's anomaly, 7 patients with Ebstein’s anomaly and 10 normal subjects were studied using phonomechanocardiography and M-mode, two-dimensional, and Doppler echocardiography. A right atrial pressure study was also performed in 4 of the 7 patients. There were 5 patients with predominant tricuspid regurgitation and 2 with a mild anomaly. A large 'c' wave was observed in the jugular venous pulse in 5 patients and in the right atrial pressure curve in 4. The upstroke of the jugular 'c' wave preceded that of the carotid arterial pulse by 35.0 ms. The interval from QRS complex onset to tricuspid valve closure was significantly longer and the closing excursion of the anterior tricuspid leaflet significantly larger in the patients than in the normal subjects. There was a trend for a positive correlation between QRS onset to jugular 'c' wave peak interval and QRS onset to tricuspid valve closure interval. The jugular 'c' wave height exhibited significant positive correlations with the size of the atrialized right ventricle and the mitral to tricuspid anulus distance, but it showed no obvious correlation with the grade of tricuspid regurgitation. These results suggest that augmentation of the jugular 'c' wave is characteristic of Ebstein's anomaly and that it correlates closely with the severity of displacement of the tricuspid valve.

Atrial natriuretic peptide in severe heart failure: Response to controlled changes in atrial pressures during intravenous nitroglycerin therapy

Atrial natriuretic peptide (ANP) levels were measured in 17 patients with severe congestive heart failure (New York Heart Association functional class IV), and the response of the peptide was studied during changes in cardiac filling pressures induced by a 24-hour infusion of nitroglycerin. In the control state plasma ANP levels (687 ± 551 pg/ml) were 10-fold normal. During the administration of nitroglycerin, natriuretic peptide levels decreased ( p < 0.005) with changes matching very closely the decreases in pulmonary arterial wedge and right atrial pressures, a 1% mean decrease in the peptide level for every 1.5 to 2% mean change in atrial filling pressures. In patients with hemodynamic tolerance to constant-dose nitroglycerin infusion, the resulting increase in atrial pressures was accompanied by an appropriate secondary increase in the plasma ANP level. During the 24-hour study period there was a direct linear relationship between both wedge ( r = 0.93, p = 0.007) and right atrial ( r = 0.93, p = 0.008) pressures and the plasma ANP level, with a zero-pressure ANP intercept near normal (69 pg/ml for wedge, 174 pg/ml for right atrial pressure). The findings were no different in a subgroup of five patients receiving simultaneous treatment with captopril, except that plasma renin activity was higher and the aldosterone level lower than in the control group by a factor of approximately 2.5. The close relationship and tracking of atrial pressure and natriuretic peptide curves suggested that the sensitivity of the atrial stretch response to changes in atrial filling pressures was maintained in severe congestive heart failure.

Determinants of Decreased Early Ventricular Filling in Man: A Role for External Forces

The determinants of reduced early left ventricular filling and their relative importance were examined in 14 subjects with an ejection fraction > 40%. Simultaneous high-fidelity left ventricular pressure, mitral annular Doppler velocity recordings, and two-dimensional echocardiographic data were used. Pressure-volume curves were created from pressure/echocardiographic/Doppler data and the chamber stiffness constant calculated. The influence of changing filling pressure was examined by studying subjects before and after ventriculography. The ventricular relaxation time constant, chamber stiffness constant, mean right atrial pressure (an index of pericardial restraint and/or ventricular interaction), pulmonary wedge pressure, and heart rate were analyzed for their influence on Doppler filling parameters: isovolumic relaxation time, peak early (E) and atrial (A) filling velocities, and the E/A ratio. The relaxation time constant was the primary determinant of isovolumic relaxation time (r = 0.82, P<0.001). Prolonged relaxation also caused a decrease in the E/A ratio (r=0.73, P<0.001) and early filling. Peak atrial filling velocity and its integral decreased as chamber stiffness rose (P<0.005). Pulmonary wedge pressure had only a modest influence on early filling (r=0.46, P<0.05). Ventriculography did not eliminate the influence of stiffness and relaxation on filling, although it caused early filling and the E/A ratio to rise and isovolumic relaxation time to shorten. Filling became earlier with increasing right atrial pressure and upward pressure-volume curve shifts. In multivariate regression the E/A ratio was influenced independently by relaxation, filling pressure, right atrial pressure, and chamber stiffness. We conclude that isovolumic relaxation time is a useful measure of ventricular relaxation. However, the E/A ratio is too complex to allow characterization of diastolic function when used alone. Finally, pericardial restraint and/or ventricular interaction during a volume load may confound the relationship between filling pattern and intrinsic ventricular diastolic properties.

Cardiopulmonary function values before and after heartworm removal in dogs with caval syndrome

SUMMARY Cardiopulmonary function values were determined before and after surgical removal of adult heartworms in 25 dogs with spontaneous and 4 dogs with drug-induced caval syndrome (cs). Fifteen dogs with spontaneous cs (recovery group) and 4 dogs with drug-induced cs (drug-induced cs group) recovered after removal, and 10 dogs with spontaneous cs were euthanatized or died (nonsurviving group). Before heartworm removal, injected radiographic contrast medium was regurgitated from the right ventricle to the right atrium. Mean pulmonary arterial pressure and total pulmonary resistance were not statistically different between the recovery and nonsurviving groups of dogs, but the end-diastolic right ventricular pressure (mean ± sd, 6.9 ±9.1 mm of Hg) and the a (8.7 ± 9.2 mm of Hg)- and v (6.3 ± 8.5 mm of Hg)-waves of the right atrial pressure curve in the recovery group were less, respectively, than the end-diastolic right ventricular pressure (17.3 ± 6.0 mm of Hg) and the a (15.8 ± 6.1 mm of Hg)- and v (21.4 ± 6.9 mm of Hg)-waves in dogs of the nonsurviving group. After heartworm removal, contrast medium regurgitation disappeared, and cardiac output of the right ventricle increased in dogs of the recovery (from 2.08 ± 0.72 to 2.38 ± 0.68 L/min; P &lt; 0.05) and drug-induced cs (from 1.42 ± 0.19 to 1.88 ± 0.26 L/ min, P &lt; 0.05) groups. However, regurgitation remained, and cardiac output did not increase in some dogs of the nonsurviving group. Mean pulmonary arterial pressure decreased significantly (from 37.7 ± 18.3 mm of Hg to 32.0 ± 16.1 mm of Hg; P &lt; 0.01) at 1 week after heart-worm removal in dogs of the recovery group, but not in those of the nonsurviving group. Total pulmonary resistance (from 12,612 ± 7,670 dynes·sec·cm-5·kg of body weight to 9,776 ± 6,089 dynes·sec·cm-5·kg; P &lt; 0.01) and right atrial pressure (a-wave: from 8.7 ± 9.2 mm of Hg to 4.1 ± 5.6 mm of Hg; v-wave: from 6.3 ± 8.5 mm of Hg to 2.1 ± 4.6 mm of Hg) decreased after heartworm removal in dogs of the recovery group. Total pulmonary resistance (from 20,309 ± 9,682 dynes·sec·cm-5·kg to 15,970 ± 6,798 dynes·sec·cm-5·kg; P &lt; 0.05) and right atrial pressure (a-wave: from 15.8 ± 6.1 mm of Hg to 10.1 ± 6.3 mm of Hg; v-wave: from 21.4 ± 6.9 mm of Hg to 11.1 ± 3.7 mm of Hg) also decreased in dogs of the nonsurviving group. However, pressures in the right side of the heart and total pulmonary resistance after heart-worm removal were greater in dogs of the nonsurviving group than in dogs of the recovery group. At necropsy, pulmonary arterial emboli containing dead heartworms were found in almost all dogs with spontaneous cs, but not in dogs with drug-induced cs. The severity of pulmonary arterial embolism correlated significantly with mean pulmonary arterial pressure before (r = 0.710; P &lt; 0.01) and 1 week after (r = 0.728; P &lt; 0.01) heartworm removal.

Cardiopulmonary values in dogs with artificial model of caval syndrome in heartworm disease.

Cardiopulmonary values were determined in dogs with an artificial model of heartworm caval syndrome, which was produced by insertion of heartworm-like silicone tubes into the tricuspid valve orifice and right atrium. Fifteen to 25 tubes with some knots were inserted in 6 dogs (knot group), and 7 to 11 tubes (small-number group) or 29 to 37 tubes (large-number group) without a knot in 3 dogs, respectively. After tube insertion, angiographic contrast medium infused into the right ventricle regurgitated to the right atrium in all cases, and the regurgitation was the most severe in the large-number group. On electrocardiographic findings, the atrial and/or ventricular premature beat developed. The height of a- and v-wave of right atrial pressure curves elevated in all groups. The elevation in v-wave was obvious in the large-number group. The pulmonary arterial pressure tended to fall or to elevate slightly, and total pulmonary resistance increased in all groups. The right cardiac output decreased significantly in all cases. The right heart hemodynamics of the model might resemble those in spontaneous cases without disturbed pulmonary circulation.

Change of left atrial systolic pressure waveform in relation to left ventricular end-diastolic pressure.

The relation between the left atrial systolic pressure waveform and left ventricular end-diastolic pressure was observed in 17 patients who underwent diagnostic cardiac catheterization. Left atrial pressure and left ventricular pressure were simultaneously recorded from a multisensor catheter before and during angiotensin infusion. Left ventricular systolic pressure and left ventricular end-diastolic pressure were 133 +/- 17 and 12.3 +/- 3.2 mm Hg, respectively, before angiotensin infusion and increased to 168 +/- 18 (p less than 0.01) and 19.4 +/- 4.5 mm Hg (p less than 0.01), respectively, during infusion. The left atrial systolic pressure curve consisted of two positive waves--a first wave (A) and a second wave (A'). The A and A' wave pressures were 11.6 +/- 2.3 and 10.2 +/- 3.9 mm Hg, respectively, before angiotensin infusion and 16.5 +/- 2.9 (p less than 0.01) and 18.1 +/- 4.7 mm Hg (p less than 0.01), respectively, during infusion. The ratio of A'/A of left atrial systolic pressure was 0.81 +/- 0.27 before angiotensin infusion and 1.08 +/- 0.14 (p less than 0.01) during infusion. The ratio of A' to A of left atrial systolic pressure was linearly related to left ventricular end-diastolic pressure before and during (p less than 0.01) angiotensin infusion. The amplitude of the A wave exceeded that of the A' wave at normal left ventricular end-diastolic pressures. However, as the left ventricular end-diastolic pressure increased either at rest or during angiotensin infusion, the amplitude of the A' wave increased and often exceeded that of the A wave. These results suggest that the second (A') wave might be attributed to the increased reflection associated with increased left ventricular end-diastolic pressure.

Atrial Standstill: An Indication For Rate Responsive Pacing

Atrial standstill (atrial paralysis) is a rare reason for permanent bradycardia. A case of atrial standstill is presented. A 35-year-old man had suffered from bradycardia since his childhood. For 2 years he had complaints (diminishment of his working capacity, and dyspnea occurred with effort) as well. On admission, a slow (38/min) junctional escape rhythm could be detected. There were no signs of atrial mechanical activity (atrial contraction) according to chest x ray, echocardiography, and the atrial pressure curve. The electrophysiological study revealed that the atria could not be electrically stimulated, and no P wave (A wave) could be recorded on right atrial electrograms. The patient received a rate responsive pacemaker. After pacemaker implantation, he became symptom-free; his working capacity improved markedly and his heart size decreased. Owing to the permanent bradycardia and the lack of atrial stimulation, the atrial standstill represents an indication for ventricular rate responsive pacing. Atrial standstill, permanent bradycardia, and the inability to stimulate the atrium are indications for ventricular rate responsive pacing.

Pressor hormones regulate atrial-stretch-induced release of atrial natriuretic peptide in the pithed rat.

Atrial wall stretching is a known stimulus for atrial natriuretic peptide (ANP) secretion. The effects of the stimulation of autonomic nervous system, hemodynamic factors, and humoral factors (epinephrine, angiotensin, vasopressin, and brain extracts) on the release of ANP under basal conditions and during increased atrial pressure produced by acute volume loading in pithed rats were examined. In conscious rats, acute volume expansion by 0.9% of saline (4 ml) increased the plasma immunoreactive ANP (IR-ANP) concentrations by a factor of 4 (140 +/- 30 pg/ml vs. 521 +/- 140 pg/ml, p less than 0.001, n = 8), whereas volume-induced ANP release was blocked in pithed rats (75 +/- 9 pg/ml vs. 99 +/- 13 pg/ml, NS, n = 7). The ANP versus right atrial pressure curve shifted to the right, indicating that much smaller amounts of IR-ANP were released in pithed than in conscious rats for each given increase in right atrial pressure. Electrical vagal and sympathetic nerve stimulation or changes in heart rate had no effect on plasma IR-ANP concentrations and failed to restore the volume-load-induced release of ANP in pithed rats. When extracts of anterior pituitary lobe, brain cortex, or hypothalamus were infused, no effect on volume-expansion-induced plasma IR-ANP levels was seen. In contrast, acute volume expansion caused a fourfold increase in levels of circulating IR-ANP in pithed rats that received posterior pituitary extracts, and the ANP versus right atrial pressure curve shifted markedly to the left. Infusion of a V1 antagonist blocked the volume-expansion-induced ANP release produced by the posterior pituitary extract. When [Arg8]-vasopressin (0.025 or 0.05 micrograms/kg/min) was infused to pithed rats, mean arterial pressure increased but basal plasma IR-ANP did not change significantly. However, acute volume expansion in the presence of vasopressin infusion (0.05 micrograms/kg/min) increased the amount of circulating IR-ANP by a factor of 4 (113 +/- 14 pg/ml vs. 414 +/- 43 pg/ml, p less than 0.001, n = 8). Thus, for a given increase in right atrial pressure, a similar amount of IR-ANP was released in the pithed rat during the vasopressin infusion as in the normal conscious animal. V1 antagonist blocked the increase in mean aterial pressure as well as the increase of plasma IR-ANP produced by [Arg8]-vasopressin. In addition, volume expansion during intravenous epinephrine (1.75 micrograms/kg/min) and angiotensin (1.0 micrograms/kg/min) doubled plasma IR-ANP levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Diagnosis of constrictive pericarditis by pulsed doppler echocardiography of the hepatic vein

The diagnostic value of hepatic venous flow patterns was evaluated for constrictive pericarditis by pulsed Doppler. A characteristic flow pattern was assumed to be associated with the well-known atrial pressure curve. Thirteen patients with constrictive pericarditis were compared to 13 control subjects and to 25 patients with right ventricular pressure overload including 13 patients with tricuspid regurgitation. The characteristic finding in constrictive pericarditis was a W-wave pattern of flow velocities in the dilated hepatic veins, with abrupt reversal of flow late in systole and diastole before the A wave (100% specificity, 68% sensitivity). This depends, however, on the absence of tricuspid regurgitation (for its systolic component) or fast sinus rhythm (for its diastolic component). Additional diagnostic markers were systolic deceleration time of forward flow (40 to 130 ms) and systolic integral of flow velocities (4.3 to 4.0 cm) (sensitivity and specificity ≥92%). In the presence of tricuspid regurgitation, diastolic deceleration time <150 ms and diastolic integral of flow velocities <6 cm were useful diagnostic signs. If combined, these criteria had 100% sensitivity and specificity for the diagnosis. Thus, pulsed Doppler assessment of flow velocities in the hepatic vein facilitates the diagnosis of constrictive pericarditis in clinical routine, using an auxiliary site with unlimited diagnostic access to the characteristic flow velocity pattern, which reflects right atrial pressure curve and filling abnormalities.

Immunoreactive atrial natriuretic peptide in ventricles, atria, hypothalamus, and plasma of genetically hypertensive rats.

To evaluate the role of extra-atrial atrial natriuretic peptide (ANP) in volume and blood pressure regulation, the plasma, atrial, ventricular, and hypothalamic levels of immunoreactive atrial natriuretic peptide (IR-ANP) were measured simultaneously in the spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) at the ages of 2, 6, and 12 months. Plasma IR-ANP in the 12-month-old, conscious SHR was significantly higher than that of the WKY (300 +/- 18 versus 200 +/- 20 pg/ml, p less than 0.05, n = 9), while no differences in plasma IR-ANP levels were found between the strains in younger rats. Acute volume expansion with saline (1.1 ml/100 g body wt) in hypertensive as well as in normotensive rats resulted in marked increases in right atrial pressure and plasma IR-ANP concentration. The older SHR had attenuated ANP release to volume loading as shown by the shift of the ANP versus right atrial pressure curve to the right. Right auricular IR-ANP concentration decreased, while that of left auricle increased with increasing age in both strains. No substantial differences were noted in auricular ANP concentration between SHR and WKY. However, the total atrial IR-ANP content (micrograms/atria) was consistently lower in SHR compared with WKY. In both ventricles, IR-ANP concentrations and contents increased with increasing age in WKY and SHR, but the ventricular levels of ANP were reduced in ventricles of the SHR heart compared with normotensive controls. The depletion of total ventricular IR-ANP was greatest in SHR with greatest ventricular hypertrophy and coincided with the attenuated ANP release to acute volume load. The increase of left but not right ventricular weight occurring secondary to 6 weeks minoxidil treatment was accompanied by higher ANP concentration in both strains. In contrast to the ventricles, the hypothalamic IR-ANP concentration was significantly increased in SHR compared with that of WKY and decreased in both strains after 6 weeks' treatment with antihypertensive drugs. Thus, ventricular and hypothalamic, as well as atrial, ANP respond to increased pressure overload in genetically hypertensive rats. Our results suggest that chronic stimulation of ANP release from ventricles is associated with depleted stores of ANP from both ventricles and reduced response to acute volume load. Our findings that ventricular ANP increased with increasing weight and in response to a hypertrophic stimulus in WKY and was decreased in SHR with severe ventricular hypertrophy suggest that ANP may locally have an inhibitory effect on the development of cardiac hypertrophy.

Continuous Measurement of Intramyocardial pH: Correlation to Functional Recovery Following Normothermic and Hypothermic Global Ischemia

The continuous measurement of intramyocardial pH was used to follow the progression of ischemia and was correlated to the recovery of left ventricular function following normothermic (38°C) and hypothermic (25°C) global ischemia. New miniature myocardial transducers, which incorporate fiberoptic technology and dual pH- and temperature-sensing capability, were placed into the left ventricular free wall and septum of 52 sheep undergoing cardiopulmonary bypass. Left ventricular stroke work as a function of mean left atrial pressure curves were generated before and after cardiopulmonary bypass by volume loading with whole blood. Functional recovery was determined by the ratio of the integrals of the preischemic and postischemic function curves. Control sheep (N = 11) did not undergo ischemia. Three groups (N = 41) underwent aortic cross-clamping until pH reached 7.0, 6.8, or 6.6. The preischemic myocardial pH averaged 7.42 ± 0.01. Following both normothermic and hypothermic global ischemia, no significant difference was demonstrated in recovery of function between control (pH 7.4) and pH 7.0 groups at either temperature. However, recovery of function of the pH 6.8 and pH 6.6 groups was significantly decreased ( p < 0.01) versus control and pH 7.0 groups at both temperatures. No significant difference in recovery of function was demonstrated at any pH level when normothermic versus hypothermic groups were compared. However, hypothermia provided increased time ( p < 0.001) before each level of function was reached with a slower rate of change of pH ( p < 0.01) compared with the corresponding same pH group in sheep undergoing normothermic (38°C) cardiopulmonary bypass. An interstitial myocardial pH lower than 7.0 at the termination of ischemia resulted in a marked decrease in left ventricular function following both normothermic and hypothermic global ischemia and reperfusion. The terminal ischemic pH value correlated to similar left ventricular functional levels of recovery at 38°C and 25°C, and rate of change of myocardial pH predicted the interval of ischemia required to achieve a given functional level of recovery.

Ventricular compliance in ischemic right ventricular dysfunction

Ischemic right ventricular dysfunction was diagnosed in 54 patients with acute myocardial infarction who had a right atrial pressure disproportionately increased in relation to the pulmonary capillary pressure. The right atrial pressure curve in 40 patients (74 percent) was M- or W-shaped, termed a noncompliant pattern, and was similar to the pattern found in constrictive pericarditis. Kussmaul's sign was found in the patients whose respiration was recorded. This pattern, which represents poor right ventricular compliance, was severe in 30 cases (y descent greater than x descent) and slight in 10 cases (y descent = x descent). Its duration was variable, ranging from days to years. Of the 54 patients, 32 (59 percent) had a low output syndrome, diagnosed in the presence of a cardiac index of less than 2.2 liters/min per m2, with signs of poor tissue perfusion. The severe noncompliant pattern was significantly related to the presence of a low output syndrome (p less than 0.01) and mortality from this cause (p less than 0.05). The jugular venous tracing pulse had a pattern similar to that of the right atrial pressure recording and therefore may be valuable in the noninvasive diagnosis of right ventricular dysfunction and in the study of the evolution of the noncompliant pattern and, hence, of ventricular compliance.

Central haemodynamics at rest and during exercise before and after combined aortic and mitral valve replacement with the Björk-Shiley tilting disc valve prosthesis.

Pre- and postoperative haemodynamics were compared in 36 patients with combined aortic and mitral valvular disease. These patients suffered from markedly restricted cardiac function in terms of cardiomegaly, low physical working capacity, hypokinetic central circulation and pulmonary hypertension. Valve replacement was performed with the Björk-Shiley Delrin disc (10) and pyrolytic carbon disc (26) prostheses and followed by subjective improvement in the majority of patients. Heart volume decreased and working capacity increased in average significantly, but were not restored to normal. The main response to surgery was a shift towards a normokinetic circulation, although many patients remained hypokinetic. There was also regression of pulmonary hypertension as a result of reduced left atrial pressure and pulmonary vascular resistance. In spite of a significant decrease in left atrial mean pressure, it remained elevated with prominent v-waves in many patients, particularly during exercise. Marked v-waves in the right atrial pressure curves were also noted in one third of the patients. Only one patient, however, suffered from clinically manifested tricuspid incompetence. This study shows the benefits of combined aortic and mitral valve replacement, even in patients with longterm haemodynamic burden on the myocardium. Although the central haemodynamics were almost normalized at rest, abnormal responses persisted during exercise.