Transesophageal echocardiographic diagnosis of right to left shunting across the foramen ovale in adults without prior stroke.

OBJECTIVES: The purpose of this study was to estimate the prevalence of potential right to left interatrial shunting and to quantify the morphologic characteristics of the fossa ovalis in adults without a prior history of stroke or systemic embolism. BACKGROUND: Paradoxic embolization through a patent foramen ovale is an important cardiac mechanism for embolic stroke. Although anatomic and physiologic data obtained by transesophageal echocardiography increase the frequency of demonstration of potential cardiac sources of systemic embolism and occasionally can conclusively demonstrate the mechanism for embolic stroke, the prevalence and prognostic implications of these findings in neurologically healthy persons are still being actively investigated. METHODS: Intraoperative transesophageal saline contrast echocardiography was performed on 50 adult patients without prior history of stroke or systemic embolism who were undergoing elective cardiovascular surgery. RESULTS: No patient had a manifest atrial septal defect by right heart oximetric measurements or transesophageal Doppler echocardiographic examination. Eleven of the 50 patients demonstrated right to left atrial passage of saline contrast medium during apnea or after release of 20-cm H2O positive airway pressure, signifying patency of the foramen ovale. These 11 patients with a patent foramen ovale had increased total excursion of the flap valve (septum primum) of the fossa ovalis (1.3 +/- 0.7 cm) compared with findings in the 39 patients without a patent foramen ovale (0.3 +/- 0.5 cm, p < 0.001). All patients with a patent foramen ovale exhibited some mobility of the septum primum and 73% of these patients had > or = 1 cm total excursion of the septum primum. In contrast, 56% of patients without a patent foramen ovale exhibited no motion of the septum primum out of the plane of the atrial septum. The maximal diameter of the fossa ovalis was greater in patients with (1.4 +/- 0.4 cm) than in patients without (1.0 +/- 0.3 cm, p < 0.003) a patent foramen ovale. CONCLUSIONS: Hypermobility of the septum primum and enlargement of the fossa ovalis are morphologic findings that occur in the presence of a patent foramen ovale.

Transesophageal echocardiographic demonstration of distinct mechanisms for right to left shunting across a patent foramen ovale in the absence of pulmonary hypertension.

The optimal visualization of the atrial septum and fossa ovalis by transesophageal echocardiography was utilized to demonstrate saline contrast transit across the atrial septum and to relate it to the motion of the flap valve (septum primum) of the fossa ovalis. In three cases, three distinct mechanisms of right to left interatrial shunting in the absence of right ventricular systolic hypertension were identified: 1) transient spontaneous reversal of the left to right atrial pressure differential with each cardiac cycle; 2) sustained elevation of right atrial pressure above left atrial pressure induced by respiratory maneuvers; and 3) aberrant flow redirection across the foramen ovale due to a large right atrial mass. Any of these three mechanisms may be operative during paradoxic embolism in the absence of elevation of right ventricular pressures.

Alterations in transesophageal pulsed Doppler indexes of filling of the left ventricle after pericardiotomy.

The impact of pericardial constraint on patterns of left ventricular filling was measured by transesophageal pulsed Doppler echocardiography in 30 patients undergoing elective nonvalvular cardiac surgery. Peak early left ventricular filling velocity increased from 0.52 +/- 0.11 to 0.56 +/- 0.15 m/s (p less than 0.05) and early left ventricular filling fraction increased from 60 +/- 9% to 65 +/- 9% (p less than 0.005) after pericardiotomy. The study group was retrospectively subdivided into two groups based on the prepericardiotomy mean right atrial pressure, an index of intrapericardial pressure and hence pericardial constraint. In 13 patients with a mean right atrial pressure less than 6 mm Hg, no significant changes in early left ventricular filling were evident after pericardiotomy. In 17 patients with a mean right atrial pressure greater than or equal to 6 mm Hg indicative of a greater degree of pericardial constraint before pericardiotomy, significant increases in peak early filling velocity (0.52 +/- 0.13 to 0.57 +/- 0.19 m/s, p less than 0.05), peak early filling rate (4.29 +/- 0.67 to 4.66 +/- 0.86 stroke volumes/s, p less than 0.05) and early left ventricular filling fraction (57 +/- 7% to 63 +/- 8%, p less than 0.001) were measured after pericardiotomy. Thus, the pericardium does constrain early left ventricular filling and its effects are more pronounced in patients with an elevated right atrial pressure.

Transesophageal echocardiographic assessment of the contribution of intrinsic tissue thickness to the appearance of a thick mitral valve in patients with mitral valve prolapse.

OBJECTIVES: This prospective, blinded transesophageal echocardiographic study was performed to determine the relative contributions of leaflet redundancy and overlap versus intrinsic tissue thickening as mechanisms for the apparent increase in diastolic thickness of the mitral valve. BACKGROUND: Increased diastolic thickness of the mitral valve has been identified as an echocardiographic feature that predicts subsequent adverse sequelae in patients with mitral valve prolapse (MVP). METHODS: Eleven patients with clinical and transthoracic echocardiographic evidence of MVP and 11 age-matched control subjects underwent protocol transesophageal echocardiography to image the mitral valve in two orthogonal planes and to measure its thickness in systole and diastole. RESULTS: Maximal diastolic width of the slack, unloaded anterior leaflet was significantly greater in patients with MVP than in control subjects (mean +/- SD: 0.64 +/- 0.20 cm vs. 0.30 +/- 0.04 cm, p < 0.001). Similarly, diastolic posterior leaflet width was greater in patients with MVP (0.67 +/- 0.39 cm vs. 0.31 +/- 0.06 cm, p < 0.01). In contrast, minimal systolic width of the distended pressure-loaded mitral valve was not significantly different between patients with MVP and control subjects for either the anterior (0.22 +/- 0.05 cm vs. 0.20 +/- 0.04 cm, p = NS) or the posterior (0.25 +/- 0.07 cm vs. 0.24 +/- 0.05 cm, p = NS) leaflets. The percent change in leaflet width from diastole to systole (% delta W), an index of the contribution of dynamic factors (e.g., leaflet redundancy and overlap) to the apparent increase in diastolic leaflet thickness, was significantly greater in patients with MVP than in control subjects for both the anterior (% delta W 62 +/- 13% vs. 34 +/- 16%, p < 0.001) and the posterior (% delta W 54 +/- 19% vs. 22 +/- 21%, p < 0.005) leaflets. CONCLUSIONS: The apparent increase in diastolic mitral leaflet thickness in patients with MVP versus control subjects is largely attributable to dynamic factors such as leaflet redundancy, overlap and deformation. During diastole, when the mitral leaflets are slack and unstressed, the leaflets appear markedly thickened in patients with MVP. In contrast, during systole, when developed intraventricular pressure distends the leaflets, causing them to stretch and balloon into the left atrium, the intrinsic tissue thickness is much less than that measured in diastole. These findings have important implications for the morphologic criteria used to diagnose MVP and the potential pathophysiologic mechanisms for adverse sequelae in this syndrome.

Segmental wall motion abnormalities in dilated cardiomyopathy: a common finding and good prognostic sign.

Fifty patients with idiopathic dilated cardiomyopathy were separated into two groups based on the presence of segmental or diffuse left ventricular wall motion abnormalities by radionuclide ventriculography. Investigation included a history and physical examination, electrocardiogram, chest X-ray film, M-mode echocardiogram, coronary angiogram and right ventricular endomyocardial biopsy. Patients with histologic evidence of myocarditis were excluded. Sixty-four percent of the patients had segmental and 36% had diffuse wall motion abnormalities. The group with segmental abnormalities showed significant differences in age (52.5 +/- 10.7 versus 37.8 +/- 14.6 years, p less than 0.001), New York Heart Association functional class III to IV (56 versus 89%, p less than 0.01), pulmonary capillary wedge pressure (14 +/- 9 versus 26 +/- 9 mm Hg, p less than 0.001), left ventricular end-diastolic dimension measured on echocardiogram (67 +/- 8 versus 77 +/- 11 mm, p less than 0.001), cardiac index (2.6 +/- 0.6 versus 2.0 +/- 0.5 liters/min per m2, p less than 0.01) and ejection fraction by radionuclide ventriculography (20 +/- 7 versus 13 +/- 5%, p less than 0.001). Patients with diffuse wall motion abnormalities had poorer histologic findings based on myocardial cell hypertrophy and nuclear changes (p less than 0.01) and a higher short-term mortality with a 1 year survival rate of 50% compared with 90% in patients with segmental wall motion abnormalities by life-table analysis (p less than 0.05). When data were reanalyzed excluding those patients with complete left bundle branch block, no significant change in any variable was detected. Segmental wall motion abnormalities, even when left bundle branch block is excluded, are common in dilated cardiomyopathy in the absence of coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

A nonsteroid anti-inflammatory drug exacerbates Coxsackie B3 murine myocarditis.

Nonsteroid anti-inflammatory drugs are often used to treat myalgias and arthralgias in enteroviral infections, but their effects on acute viral myocarditis are unknown. The effect of the nonsteroidal anti-inflammatory drug, ibuprofen, on acute viral myocarditis was studied in 75 four week old male BALB/c mice infected with 1.75 X 10(7) plaque-forming units of Coxsackie virus B3 on day 0. Ibuprofen was given intraperitoneally at a dose of 15 mg/kg body weight daily. The mice were assigned to four groups--Group I, 18 uninfected mice given ibuprofen on days 1 to 14; Group II, 18 infected, untreated mice; Group III, 20 infected mice given ibuprofen on days 1 to 14; and Group IV, 17 infected mice given ibuprofen on days 7 to 14. Nine animals in Group I, eight in Group II and seven in Group III were killed on day 7; the remaining mice were killed on day 14. Heart viral cultures and histologic analysis were done. Cultures at days 7 and 14 were all negative. Inflammation and necrosis analyzed in each animal were graded 0 to 4, with grade 4 representing widespread inflammation and necrosis. The heart was histologically normal in all 18 uninfected mice (Group I) given ibuprofen only. Inflammation and necrosis were not significantly different in Group II (infected, untreated) and Group III (infected, treated beginning day 1) mice killed at day 7. Inflammation scores of mice killed on day 14 were 2.1 +/- 0.6 (Group II), 3.1 +/- 0.7 (Group III) and 2.9 +/- 1.0 (Group IV infected, treated days 7 to 14).(ABSTRACT TRUNCATED AT 250 WORDS)

Peripartum cardiomyopathy: clinical, hemodynamic, histologic and prognostic characteristics.

Peripartum cardiomyopathy is defined as left ventricular dilation and failure, first developing during the third trimester of pregnancy or in the first 6 months postpartum. In an effort to characterize this syndrome in a middle class population, 14 consecutive patients with peripartum cardiomyopathy underwent a detailed history and physical examination, right heart catheterization, M-mode and two-dimensional echocardiography, radionuclide ventriculography and right ventricular endomyocardial biopsy. These patients were then observed with sequential noninvasive studies to determine prognostic indicators. Eight (57%) of these 14 patients were primiparous and an equal number first presented with heart failure concomitant with or immediately before the onset of labor. When these women were compared with 55 patients with idiopathic dilated cardiomyopathy, only mean age at onset of symptoms (28.7 +/- 5.7 versus 48.2 +/- 13.6 years, p less than 0.001) and symptom duration (4.1 +/- 7.7 versus 19.0 +/- 18.4 months, p less than 0.001) differed between the groups. There was no difference in ventricular arrhythmia, left ventricular chamber size, ejection fraction or hemodynamics. Myocyte histologic findings were similar; however, myocarditis was identified in 29% of patients with peripartum cardiomyopathy and in only 9% of those with idiopathic dilated cardiomyopathy. In all patients with peripartum cardiomyopathy and myocarditis, the myocardial biopsy was performed within 1 week of onset of symptoms. Seven (50%) of the patients with peripartum cardiomyopathy had dramatic improvement within 6 weeks of follow-up, and 6 (43%) died.(ABSTRACT TRUNCATED AT 250 WORDS)

"Stunning" of the left atrium after spontaneous conversion of atrial fibrillation to sinus rhythm: demonstration by transesophageal Doppler techniques in a canine model.

OBJECTIVES: This study compared left atrial and left atrial appendage contraction velocities in sinus rhythm before and after a brief period of atrial fibrillation in a canine model. BACKGROUND: In patients, left atrial appendage contraction velocities measured during sinus rhythm after cardioversion from atrial fibrillation are depressed relative to left atrial appendage emptying velocities measured during atrial fibrillation, suggesting that the left atrial appendage is mechanically "stunned." METHODS: This phenomenon was studied in a canine model of acute (60 min) pacing-induced atrial fibrillation followed by spontaneous reversion to sinus rhythm using epicardial and transesophageal pulsed wave Doppler. Unique features of the model include: 1) comparison of left atrial function postconversion to baseline sinus rhythm rather than to measurements during atrial fibrillation, 2) control of the duration of atrial fibrillation and 3) elimination of the extraneous influences of direct current shock and antiarrhythmic agents, which may independently depress left atrial function. RESULTS: Hemodynamic conditions (heart rate, mean arterial pressure, cardiac output, mean pulmonary artery pressure, mean right atrial pressure and mean left atrial pressure) at baseline, during 60 min of atrial fibrillation and after reversion to sinus rhythm were constant throughout the study period. Peak left atrial contraction velocities (measured from the transmitral flow velocity profile) were significantly (p < 0.02) reduced to 64+/-22% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 20 min after resumption of sinus rhythm. Peak left atrial appendage contraction velocities were significantly (p < 0.001) reduced to 49+/-24% of baseline values upon spontaneous conversion of atrial fibrillation to sinus rhythm and recovered to basal values by 40 min after reversion to sinus rhythm. CONCLUSIONS: Even brief (60 min) periods of atrial fibrillation in normal canine hearts result in marked depression of global left atrial systolic function and regional left atrial (left atrial appendage) systolic function upon resumption of sinus rhythm. This "mechanical stunning" of left atrial systolic function appears to be more profound and of longer duration for the left atrial appendage compared with the left atrium as a whole, which may predispose the appendage to blood stasis and thrombus formation. Chronic models of atrial fibrillation need to be developed to examine the impact of longer periods of atrial fibrillation upon the magnitude and duration of postconversion left atrial "stunning."

Treatment of cardiogenic shock in myocardial infarction by intraaortic balloon counterpulsation surgery.

Thirty-seven patients in cardiogenic shock due to acute myocardial infarction were treated with intraaortic balloon counterpulsation and/or surgery. Eighteen of these patients were treated with counterpulsation alone; eight survived and five were in functional class I or II at the time of follow-up; two were in functional class III, and one was in functional class IV. Nineteen patients were treated surgically, eight survived and seven were in functional class I or II at the time of follow-up; one was in functional class III. Good functional recovery with counterpulsation alone is most common with inferior infarction. With surgery, functional recovery depends not only on the extent of the infarction and the coronary anatomy, but also on the ability to perform surgery within 12 hours of infarction or to support the patient with mechanical means for 10 to 14 days after the infarction and then perform surgery.

Mechanism of the effect of bretylium on the ventricular fibrillation threshold in dogs.

Experiments were performed to determine the importance of sympathetic blockade vs a direct myocardial effect as a mechanism for the antifibrillatory action of bretylium. The ventricular fibrillation (VF) threshold was determined in open-chest, anesthetized dogs by scanning the vulnerable period with either a single electrical stimulus (10 ms) or a train of electrical stimuli (14 pulses, 4 ms, 100 Hz). Using the train-of-pulses technique, the VF threshold increased from 6.8 +/- 0.6 mA to 29.7 +/- 6.4 mA 15 minutes after a 10-mg/kg intravenous bolus of bretylium (p less than 0.001, n = 8). There was no further significant change in the train-of-pulses VF threshold at 2 or 4 hours. Beta-adrenergic blockade with timolol (0.2 mg/kg) increased the train-of-pulses VF threshold from 6.7 +/- 1.6 mA to 24.5 +/- 5.2 mA (p less than 0.01 n = 8) and prevented any further significant change in response to bretylium. When single electrical pulses were used to scan the vulnerable period, bretylium at doses of 10 mg/kg (n = 8) and 100 mg/kg (n = 6) did not alter the VF threshold over a 4-hour observation period. The administration of timolol, alone or in combination with bretylium, did not significantly alter the single-pulse VF threshold. The failure of bretylium to alter the single-pulse VF threshold was not dependent on the site of stimulation. Stimulation of the right sympathetic cardiac nerves showed that 15 minutes of bretylium treatment was sufficient to completely inhibit adrenergic neuronal transmission to the myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Safety and efficacy of esmolol for unstable angina pectoris.

Esmolol is a rapidly metabolized cardioselective beta-adrenergic blocker that provides steady state beta-adrenergic blockade when administered by continuous intravenous infusion. To determine the efficacy of esmolol in the management of unstable angina, 23 patients with known coronary artery disease, who averaged 3.7 +/- 2.7 daily episodes of chest pain at rest, were randomized to receive either a continuous infusion of esmolol (n = 12) or oral propranolol (n = 11), as an adjunct to concomitant antianginal therapy. Patients with systolic blood pressure less than 110 mm Hg, heart rate less than 60 beats/min or known contraindications to beta blockade were excluded. Esmolol was titrated in a step-wise fashion from 2 to 24 mg/min at 5-minute intervals up to a 30% reduction in heart rate and systolic blood pressure double-product. The propranolol dose was increased every 6 hours by 50 to 100% to achieve a similar reduction in heart rate and blood pressure. When compared with their 24-hour baseline periods, both groups achieved a significant reduction in episodes of chest pain, from 4.6 +/- 3.3 to 1.4 +/- 1.5 in the esmolol group (p less than 0.02) and 2.6 +/- 1.4 to 1.0 +/- 1.5 in the propranolol group (p less than 0.02) during the subsequent study period. The cardiac event rate and incidence of drug side effects were similar between the 2 groups; however, side effects seen with esmolol did not require treatment after drug discontinuation. Thus, maximally tolerated beta blockade is an effective therapy for unstable angina.(ABSTRACT TRUNCATED AT 250 WORDS)

Digoxin and the susceptibility of the canine heart to countershock-induced arrhythmia.

This study investigated the effects of therapeutic and subtoxic doses of digoxin on the risk of ventricular tachycardia (VT) after graded, transthoracic shocks in anesthetized dogs. A series of direct current shocks (5, 10, 25, 50, 75, 100, 150 and 200 J) was delivered to 33 normal dogs and 6 dogs with a healed (32 +/- 7 days) myocardial infarct (MI). In 10 untreated dogs, the duration of post-shock VT was highly reproducible when 3 separate series of shocks were delivered at 2-hour intervals. In 6 normal dogs treated with oral digoxin (0.5 mg/day for 5 to 7 days), a series of shocks delivered before and during treatment (serum levels 1.5 +/- 0.5 ng/ml) resulted in the same duration of post-shock VT. In 18 normal and 6 dogs with MI, a series of shocks was given before and 90 minutes after a therapeutic dose of digoxin (0.05 mg/kg intravenously). At this dose of digitalis (serum level 2.5 +/- 1.0 ng/ml), there was no difference in the duration of post-shock VT in either normal dogs or dogs with MI. A third series of shocks was given after achieving subtoxic digitalization with additional intravenous digoxin (0.01 mg/kg) every 30 minutes until a premature ventricular stimulus evoked a repetitive ventricular response. The subtoxic doses of digitalis (serum levels 13.9 +/- 4.7 ng/ml) increased the duration of post-shock VT in both normal dogs (100%) and dogs with MI (700%) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of indomethacin on coronary hemodynamics, myocardial metabolism and anginal threshold in coronary artery disease.

The effects of orally administered indomethacin or placebo on coronary hemodynamics were studied in 23 patients with coronary artery disease. After indomethacin administration the systemic arterial pressure increased by 12 +/- 4% and the myocardial oxygen consumption by 24 +/- 11%. Coronary sinus flow did not change and coronary vascular resistance increased slightly. Oxygen saturation of the arterial blood did not change, but coronary sinus saturation decreased substantially. Hemodynamic values returned to normal 150 minutes after administration of indomethacin. During rapid atrial pacing, coronary sinus flow increased 79 +/- 14% above the rest value when pacing was done before indomethacin administration; only a 56 +/- 12% increase was seen when pacing was repeated after indomethacin. Peak heart rate achieved during atrial pacing, severity of angina and the degree of ST-segment depression were not altered by indomethacin treatment. Orally administered indomethacin has a mild coronary vasoconstrictive effect that does not interfere substantially with the expected increase in myocardial blood flow during rapid atrial pacing. Anginal threshold is not altered by orally administered indomethacin.

Ventricular fibrillation during coronary angiography in dogs: the role of calcium-binding additives.

Coronary angiography with Renografin 76 (RG76) occasionally results in ventricular fibrillation (VF). Angiovist 370 (AV370) is a contrast medium similar to RG76 except the calcium-sequestering agents, sodium citrate and EDTA in RG76 have been replaced by calcium EDTA. To determine whether these sequestering agents contribute to contrast medium-induced VF, a comparison was made of the effects of intracoronary injections of RG76, AV370, and saline solutions containing sodium citrate and EDTA (CIT/EDTA) and calcium EDTA (CA EDTA) on myocardial conduction, local QT intervals, and incidence of spontaneous and induced VF in 32 dogs. Four milliliters of RG76 produced a 111 +/- 12-ms increase in local QT intervals, compared with a 73 +/- 8-ms increase with AV370 (p less than 0.001). Spontaneous VF occurred in 12 of 16 six-milliliter injections of RG76, compared with 4 of 16 injections of AV370 (p less than 0.02) An early-cycle premature impulse applied after every fourth beat induced VF in 15 of 16 four-milliliter injections of RG76 compared with 5 of 16 injections of AV370 (p less than 0.01). As the premature beat conducted through the left anterior descending region, conduction slowing and fractionation occurred, which was less with AV370 than with RG76. The CIT/EDTA solution produced a greater increase in QT intervals (77 +/- 5 ms) than the CA EDTA solution (29 +/- 3 ms) or 0.9% saline solution alone (28 +/- 2 ms) (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Beta blockers and the sensitivity of the thallium treadmill test.

The effect beta blockers (BB) may have on the sensitivity of the thallium treadmill test (Th-TMT) is controversial. The purpose of this study was to test the hypothesis that BB decrease the sensitivity of the Th-TMT. Two hundred three patients over a two-year period were identified who satisfied the following criteria. All had symptom-limited upright treadmill exercise tests with stress and redistribution thallium imaging, as well as coronary angiography within two months of the Th-TMT. Of 58 patients with CAD not on BB, 52 had an abnormal Th-TMT scan (sensitivity 90 percent). In comparison, the sensitivity of the Th-TMT scan in the 88 patients with CAD receiving BB was 76 percent (p less than 0.05). We conclude that BB may significantly decrease the sensitivity of the Th-TMT. Physicians should fully appreciate the higher false negative rate (24 vs 10 percent) for patients on BB and consider cautious withdrawal prior to diagnostic studies.

The effects of rapid volume expansion on the right and left cardiac filling pressures after coronary artery bypass surgery.

Rapid volume expansion is a diagnostic procedure which can reveal typical hemodynamics of pericardial constriction in patients with pericardial disease who have normal hemodynamics in their baseline state. We studied 20 patients with previous coronary artery bypass surgery in order to determine whether this operation results in some degree of pericardial constriction which could be demonstrated by rapid volume expansion. After infusing 1 L of physiologic saline solution over six minutes, the right atrial pressure increased by 5 +/- 2 mm Hg, the right ventricular diastolic pressure by 4 +/- 3 mm Hg, the pulmonary capillary wedge pressure by 7 +/- 3 mm Hg, and the left ventricular diastolic pressure by 7 +/- 4 mm Hg (mean +/- SD). Equalization of the left and right cardiac pressures was not observed, and the normal respiratory variation of the pressures was not altered by rapid volume expansion. Thus, the pericardial manipulation associated with the performance of coronary artery bypass surgery does not commonly result in the development of subclinical pericardial constriction.

Management of left ventricular rupture complicating myocardial infarction.

Rupture of the left ventricle secondary to myocardial infarction may occur more often than is suspected. More time than anticipated may be available between rupture and catastrophic deterioration. Hemodynamic stabilization, diagnostic studies, and surgical treatment can be successfully undertaken. Four patients have been successfully treated in our institution. Rupture occurred from 1 to 14 days after infarction. Persistent chest pain was present in all. All were hemodynamically unstable and all stabilized with counterpulsation. One patient was in cardiogenic shock, two had a cardiac arrest, and one presented with cardiac tamponade requiring two emergency pericardiocenteses. Coronary arteriography was done in all four patients. Surgical management consisted of infarctectomy and repair of the ventricular rupture. Additionally, a single aortacoronary bypass graft was needed in two patients and repair of a ventricular septal rupture was necessary in a third. There was no operative mortality. One patient drowned 1 year later. We conclude that successful surgical management requires (1) suspicion of ventricular rupture, (2) hemodynamic stabilization by counterpulsation, (3) coronary arteriography, and (4) combined infarctectomy and repair with revascularization.

Contrast media-induced ventricular fibrillation. A comparison of Hypaque-76, Hexabrix, and Omnipaque.

Contrast media occasionally produce ventricular fibrillation during coronary angiography. We compared the fibrillatory propensity of the conventional ionic contrast medium, Hypaque-76 (H76) to the low osmolar ionic dimer Hexabrix (HB) and to the nonionic agent Omnipaque (OM) in 20 open chest anesthetized dogs. Intracoronary injection of 6 mL of contrast medium produced spontaneous ventricular fibrillation in four of ten dogs with H76, compared with two of ten with HB, and zero of ten with OM (P = .07). The induction of two premature beats by programmed stimulation of the myocardium during injection of 4 mL of contrast medium produced ventricular fibrillation in ten of ten dogs with H76, compared with three of ten with HB, and zero of ten with OM (P less than .001). Both H76 and HB produced ventricular fibrillation in ten of ten dogs when three premature beats were induced, compared with two of ten dogs with OM (P less than .001). Four mL H76 produced a 109 +/- 18 msec increase in the QT interval, compared with an 82 +/- 17 msec increase with HB, and a 45 +/- 12 msec increase with OM. We conclude that both low osmolar HB and OM are less fibrillatory than the conventional ionic medium H76, and that the nonionic medium OM is less fibrillatory than the ionic dimer contrast medium HB.

The effect of sodium on the fibrillatory propensity of nonionic contrast media.

Removing sodium from standard ionic contrast media markedly increases the incidence of ventricular fibrillation in patients undergoing coronary angiography. Newer nonionic contrast media, iopamidol, iohexol, and ioversol contain only trace amounts of sodium. To determine whether sodium attenuates or potentiates ventricular fibrillation from nonionic contrast media, we measured the prolongation in QT interval and performed programmed electrical stimulation with one, two and three extra ventricular stimuli in 40 dogs during 4-mL intracoronary injections of iopamidol, iohexol, and ioversol. Solutions of each contrast medium with added NaCl at concentrations of 0.225%, 0.45%, and 0.9% were compared with standard contrast media. The addition of NaCl markedly increased the amount of QT interval prolongation produced by each contrast medium. With iopamidol, the amount of QT interval prolongation was 40 +/- 11 msec with standard iopamidol, but was 58 +/- 11 msec with 0.225% NaCl/iopamidol, 84 +/- 17 msec with 0.45% NaCl/iopamidol, and 132 +/- 42 msec with 0.9% NaCl/iopamidol (P less than .001). Similar results were seen with iohexol and ioversol. Ventricular fibrillation was difficult to induce with standard solutions of these agents (even with three extra stimuli), but became progressively easier to induce when NaCl was added. Three extra stimuli produced ventricular fibrillation in zero of 11 dogs with standard iopamidol, zero of 11 with 0.225% NaCl/iopamidol, three of 11 with 0.45% NaCl/iopamidol, and eight of 11 with 0.9% NaCl/iopamidol (P less than .001). Similar results were observed with iohexol and ioversol. The addition of choline chloride or dextrose did not increase ventricular fibrillation and QT interval prolongation. It is concluded that standard preparations of nonionic contrast media have a very low fibrillatory propensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of intracoronary administration of contrast media on myocardial high-energy phosphate. A comparison of sodium meglumine diatrizoate and iohexol.

Myocardial ATP, ADP, and AMP were measured from cardiac biopsy in 11 dogs after intracoronary injection of 6 mL of sodium-meglumine diatrizoate (SMD), iohexol (IOH), or 0.9% sodium chloride (NaCl), and in three of the dogs at baseline before any injection. The ATP at baseline and after SMD, IOH, and 0.9% NaCl were 5.39 +/- 0.41, 3.72 +/- 0.70, 5.52 +/- 0.82, and 5.44 +/- 1.40 mumol/g wet weight, respectively. There were significant differences between SMD and IOH (P less than .02), and between SMD and 0.9% NaCl (P less than .05). The energy charge of SMD was 0.82 +/- 0.08, which differed from 0.89 +/- 0.02 for NaCl or 0.9 +/- 0.05 for baseline (P less than .05), but not from 0.85 +/- 0.04 for IOH. In conclusion, diatrizoate caused significant depletions in ATP stores in comparison with iohexol, but there was no significant difference with respect to energy charge. Nonionic contrast media would be preferable for coronary arteriography in patients whose high-energy stores might be depleted from severe ischemia.