Potential limitations of percutaneous transluminal coronary angioplasty in heart transplant recipients.
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Biomedical subjects
Publications and source records attributed to B F Uretsky.
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Timing of surgical repair of ventricular septal defect developing after acute myocardial infarction remains controversial. We report the case of a 75-year-old man in whom a ventricular septal defect developed 7 days after myocardial infarction. The patient was maintained on intraaortic balloon pump support for 33 days before successful surgical closure. In the present era of aggressive preoperative hemodynamic management, the strategy of prolonged support before definitive operation on patients with myocardial infarction in whom a ventricular septal defect develops must be reconsidered.
The goal of this study was to evaluate the relative contribution of the renin-angiotensin system and mean arterial pressure to sodium excretion and urine flow rate during an infusion of atrial natriuretic peptide (ANP) at physiologically relevant doses in humans. Eight normal volunteers were studied during five periods: (1) baseline in the supine position; (2) during an infusion of ANP at physiologic doses (0.01 micrograms/kg/min) in the supine position; (3) during ANP infusion and 60 degrees head-up tilt; (4) during ANP infusion, head-up tilt, and interruption of the renin-angiotensin axis with the angiotensin converting enzyme inhibitor (ACEI) enalaprilat; and (5) in the supine position during ANP infusion and ACEI. Infusion of ANP in the supine posture significantly increased urine flow rate and sodium excretion compared to baseline while mean arterial pressure and plasma renin activity were unchanged. During head-up tilt and ANP infusion, urine flow rate and sodium excretion were no longer significantly elevated over baseline while mean arterial pressure decreased and plasma angiotensin II levels increased. Addition of ACEI caused a marked diminution of urine flow rate and sodium excretion compared to baseline levels despite continued ANP infusion. Although mean arterial pressure after ACEI administration was lower than baseline, it was not significantly different from the non-ACEI head-up tilt state. Placing subjects in the supine position during ANP infusion and ACEI administration increased mean arterial pressure to levels that were no longer different from baseline, but urine flow rate and sodium excretion remained significantly depressed to the same degree as during head-up tilt with ACEI.(ABSTRACT TRUNCATED AT 250 WORDS)
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Peak filling rate is an indicator of left ventricular (LV) diastolic function. It is influenced by heart rate, loading conditions, sympathetic nervous system activity, ejection fraction and other factors. To determine the effect of altered loading conditions on peak filling rate, independent of heart rate and sympathetic nervous system activity, 12 patients were studied 3 weeks after orthotopic heart transplantation. Plasma catecholamine level, heart rate and ejection fraction were not changed by any maneuver. Nitroglycerin caused a decrease in pulmonary artery wedge pressure (9 +/- 2 to 6 +/- 1 mm Hg, p less than 0.001) and in absolute peak filling rate (46.0 +/- 3.0 to 42.8 +/- 2.5 kcts/s, p less than 0.01), but no change in normalized peak filling rate. Volume infusion increased pulmonary artery wedge pressure (9 +/- 2 to 12 +/- 2 mm Hg, p less than 0.001) and absolute peak filling rate (46.0 +/- 3.0 to 51.5 +/- 5.3 kcts/s, p less than 0.01), but peak filling rate normalized to stroke volume was unchanged. During nitroglycerin and volume infusions, there was a high correlation between changes in pulmonary artery wedge pressure and absolute peak filling rate (r = 0.82, p less than 0.001). With normalization of peak filling rate, these variables correlated less well. With methoxamine, 4 patients demonstrating systolic dysfunction had a decrease in absolute and normalized peak filling rate despite a large increase in pulmonary artery wedge pressure. The other 8 patients without systolic dysfunction had an increase in pulmonary artery wedge pressure with increased absolute but unchanged normalized peak filling rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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Prolonged, continuous intra-aortic balloon (IAB) counterpulsation for several weeks can result in balloon entrapment secondary to thrombus formation in the balloon lumen. In this report, we describe a patient who developed IAB entrapment, early (1 wk) after initiation of counterpulsation. A trace amount of blood was noted in the tubing connecting the balloon catheter to the console for 3 days prior to IAB malfunction and vascular entrapment. We suggest that the balloon catheter be removed immediately when blood is detected in the external connecting tubing even if the IAB is functioning satisfactorily.
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Congestive heart failure patients with severe pulmonary hypertension are at risk of death from acute right ventricular failure of the donor heart in the early postoperative period after orthotopic cardiac transplantation. Therefore in the preoperative evaluation of these patients, it is extremely important to determine whether pulmonary hypertension can be reversed by pharmacologic means. Patients with reactive pulmonary hypertension can be considered suitable for orthotopic transplantation and the effective drug utilized postoperatively to reverse pulmonary hypertension and prevent failure of the donor right ventricle. To determine which pharmacologic agent is most effective in reversing pulmonary hypertension in congestive heart failure, the acute pulmonary hemodynamic effects of comparable doses of direct intravenous vasodilators including nitroglycerin, nitroprusside, and prostaglandin E1, and intravenous inotropic agents dobutamine and enoximone, were evaluated in 66 patients undergoing cardiac transplantation evaluation. All drugs significantly increased cardiac output and decreased calculated pulmonary vascular resistance. All drugs except dobutamine significantly lowered pulmonary artery and pulmonary artery wedge pressures. Prostaglandin E1 was the only drug that significantly lowered transpulmonary pressure gradient (pulmonary artery mean pressure minus mean pulmonary wedge pressure). The magnitude of decline of pulmonary vascular resistance and transpulmonary pressure gradient was greatest with prostaglandin E1 compared with other drugs. These observations indicate that prostaglandin E1 may be more effective than the other studied drugs for acute reversal of pulmonary hypertension in congestive heart failure.
To evaluate potential physiological actions of atrial natriuretic peptide (ANP) in humans, normal male volunteers were studied in the supine and head-up tilt positions both in the absence and presence of an ANP infusion at a rate which increased plasma ANP levels to ranges observed during physiological stimuli such as volume expansion. Infusion of ANP in the supine position provoked a significant natriuresis and diuresis and suppressed aldosterone secretion. Head-up tilt alone caused expected decreases in urine flow rate and the absolute and fractional excretion rates of sodium and increases in plasma renin activity and aldosterone levels. The combination of head-up tilt and ANP infusion resulted in a less marked decrease in urine flow rate and sodium excretion and a similar increase in plasma renin activity. However, there was a significant decrease in plasma aldosterone levels. These data support a physiologic action of ANP on renal and adrenal function.
OBJECTIVE: To evaluate whether underlying anatomical variations in the position of the internal jugular vein may account for difficulty in obtaining central venous access in individual patients. DESIGN: Consecutive series. SETTING: Cardiac catheterization laboratory, coronary care unit, and ICU. PATIENTS: Two hundred patients (52 +/- 7 yrs, 147 males) who were undergoing internal jugular vein cannulation for hemodynamic monitoring or endomyocardial biopsy. INTERVENTION: The internal jugular vein and carotid artery were visualized with two-dimensional ultrasound and their position was compared with their projected location from external landmarks. RESULTS: In 183 (92%) patients, the position of the internal jugular vein was lateral and anterior to the carotid artery and increased in diameter during a Valsalva maneuver. In five (2.5%) patients, the internal jugular vein was not visualized and was probably thrombosed, as the internal jugular vein was normal on the other side. In six (3%) patients, the internal jugular vein was unusually small and did not increase in diameter during the Valsalva maneuver. In two (1%) patients, the internal jugular vein was positioned greater than 1 cm lateral to the carotid artery. Four (2%) patients had a medially positioned internal jugular vein overlying the carotid artery. In 5.5% of the patients, the position of the internal jugular vein was outside the path that had been predicted by the external landmarks. CONCLUSIONS: These findings suggest that anatomical variation may partly account for the inability to cannulate the internal jugular vein in certain patients. In these cases, ultrasound examination quickly establishes the position of the internal jugular vein and may allow for easy and rapid access.
Percutaneous transluminal coronary angioplasty was performed at the time of the diagnostic catheterization in 188 patients (215 lesions) at a University Hospital in order to assess the efficacy of this approach and the potential role it should play in the evaluation and treatment of patients. Patients either presented for diagnostic catheterization for evaluation of stable coronary disease (79 patients) or for unstable or new onset anginal symptoms (109 patients). Lesions were graded as to whether they were simple or complex; and post angioplasty films were reviewed for success rate, and degree of revascularization. Patients who were referred for stable anginal symptoms had a slightly higher success rate (91%) compared to those who were referred for new onset or more unstable symptomatology (85%, p = ns). Additionally, lesions morphology was judged to be more complex in unstable patients, as 67% had complex lesions with the presence of thrombus or ulcerated plaque in 56% of these stenoses. Angioplasty success was high for simple lesions in all patients, but was most unfavorable for complex stenoses in patients who presented with unstable symptoms (81% success rate). In patients who presented with new onset or unstable symptoms multivessel disease was present in 69% and angioplasty was more often geared at dilating a culprit stenosis leaving only 49% of these patients with complete revascularization. On the other hand, in 76% of those patients who presented with stable angina complete revascularization was a common outcome. Length of hospital stay was considerably shorter at 2.9 +/- 0.8 days in those patients who presented with stable symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a patient with ischemic cardiomyopathy who was treated with a continuous high dose infusion of intravenous nitroglycerin for six months while awaiting cardiac transplantation. Surprisingly, methemoglobinemia did not develop and nitroglycerin continued to be clinically effective in relieving angina during the six-month period. We believe this to be the first reported instance of the safe use of such prolonged infusion of intravenous nitroglycerin.
When examining survival rates following cardiac transplantation, it is important to examine the risk factors for both early (30-day) and late (greater than 30-day) survival as they may well be different. Factors affecting early survival appear related more to the preoperative condition of the patient (including degree of pulmonary hypertension) as well as advances that have been made in postoperative care. It is not immediately obvious why gender has such a profound effect on early survival and why primary graft failure rates appear higher in this group. Donor organ factors did not appear to relate to this difference. On the other hand, late survival appears to be influenced mainly by immunologic factors such as panel reactive antibody level and immunosuppressive protocol. A less dramatic effect of transpulmonary gradient appears to have a lasting effect on recipients even when they survive the initial 30-day period. Thus, pulmonary hypertension may have prolonged effects on the cardiac allograft which as yet we do not understand completely. The majority of late mortality is still due to graft atherosclerosis, infection, and acute cellular rejection, the latter 2 occurring most frequently within the first year after transplantation whereas death from graft atherosclerosis becomes most prominent beyond 5 years. Despite persistent improvements in 30-day survival, late survival following cardiac transplantation will only improve with the advent of better tissue matching and improved immunosuppression. The results with FK506, for example, are promising.
Amyloid heart disease has been considered a contraindication for cardiac transplant based on the hypothesis that it is a systemic disease and that amyloid deposition would occur in the cardiac allograft. A survey was sent to all of the US centers and a limited number of Canadian and European centers listed with the International Registry. Twenty-four centers responded, and data were ultimately provided for a total of 10 patients (3 men, 7 women, mean age 48 years, range 30-60 years) who were transplanted for cardiac amyloid. The diagnosis of cardiac amyloidosis was made histologically on endomyocardial biopsy and/or examination of the explanted heart. Additional documented organ involvement included liver (two of 10), rectal (three of 10), renal (two of 10), gingiva (two of 10), and tongue (one of 10), although invasive biopsies were not performed in a majority of patients. A specific amyloid protein was identified in eight patients (seven lambda, one kappa immunoglobulin light chain). Although four of the surviving nine patients (one perioperative death) developed recurrent amyloid deposition in the allograft, it was detected solely by electron microscopy in two of these and had no clinical significance. There was, however, a progressive risk of major organ involvement with organ function impairment in this group (22% at 12 months, 50% at 24 months, 66% at 48 months). Although the immediate and early postoperative outcomes were not dissimilar between this group and patients undergoing transplantation for other cardiac diseases, late survival was reduced (39% at 48 months) compared with the larger population, but differences were not statistically significant due to the small amyloid sample size (p = 0.16).(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the pathophysiology of cardiac tamponade, the hemodynamics of 77 consecutive patients with greater than 150 ml of pericardial effusion were studied. Patients were classified into 3 groups based on the equilibration of intrapericardial with right atrial and pulmonary arterial wedge pressures (mm Hg): group I (n = 16), intrapericardial pressure was less than right atrial and pulmonary arterial wedge pressures; group II (n = 13), intrapericardial pressure was equilibrated with right atrial but not pulmonary arterial wedge pressures; group III (n = 48), intrapericardial pressure was equilibrated with right atrial and pulmonary arterial wedge pressures. Pericardiocentesis produced the following changes: group I--significant (p less than 0.03) decreases in intrapericardial pressure (7 +/- 2 mm Hg), right atrial pressure (3 +/- 2 mm Hg), pulmonary arterial wedge pressure (2 +/- 2 mm Hg), and the inspiratory decrease in arterial systolic pressure (3 +/- 4 mm Hg) but no significant change in cardiac output; group II--significant (p less than 0.02) decreases in intrapericardial pressure (11 +/- 5 mm Hg), right atrial pressure (6 +/- 4 mm Hg), pulmonary arterial wedge pressure (4 +/- 5 mm Hg), and inspiratory decrease in arterial systolic pressure (8 +/- 7 mm Hg), and increase in cardiac output (1.1 +/- 1.2 liters/min); group III--significant (p less than 0.001) decreases in intrapericardial pressure (16 +/- 7 mm Hg), right atrial pressure (9 +/- 4 mm Hg), pulmonary arterial wedge pressure (8 +/- 5 mm Hg), inspiratory decrease in arterial systolic pressure (17 +/- 11 mm Hg), and increase in cardiac output (2.8 +/- 1.5 liters/min). The changes after pericardiocentesis in all parameters were significantly (p less than 0.05) greater in group III than in groups I or II except for the change in right atrial pressure, which was not significantly different in groups II versus III. The changes after pericardiocentesis indicate pericardial effusion caused the greatest abnormalities in group III but also caused significant abnormalities of pressure and flow in group II and of pressure alone in group I.(ABSTRACT TRUNCATED AT 250 WORDS)
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