Rotational coronary ablation: more grist for the interventional mill?
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
R Bach
Publications and source records attributed to R Bach.
Augmentation of coronary blood flow by intra-aortic balloon pumping in patients after coronary angioplasty.
BACKGROUND: Controversy exists regarding the ability of intra-aortic balloon pumping to increase coronary blood flow in patients with obstructive coronary artery disease. To assess the effects of intra-aortic balloon pumping on coronary hemodynamics, we measured coronary blood flow velocity with a 0.018-in. Doppler-tipped angioplasty guide wire in 15 patients who received an intra-aortic balloon pump for typical clinical indications. METHODS AND RESULTS: Intra-aortic balloon pumping augmented diastolic pressure 83 +/- 35%. In nine patients before angioplasty, peak diastolic coronary flow velocity beyond the stenosis (mean diameter narrowing, 95 +/- 7%) was 5.3 +/- 9.6 cm/sec and was unaffected by intra-aortic balloon pumping. After angioplasty, the improved coronary luminal diameter narrowing (n = 12; mean narrowing, 18 +/- 12%) was associated with increased distal diastolic flow velocity integral and peak diastolic and mean velocities (13.3 +/- 8.4 units: 36.4 +/- 18.3 and 24.0 +/- 11.4 cm/sec, respectively; all p < 0.01 versus before angioplasty), which were further augmented (36 +/- 37%, 54 +/- 49%, and 26 +/- 17%, respectively; all p < 0.01) with intra-aortic balloon pumping. Intra-aortic balloon pumping did not significantly increase the distal systolic velocity integral (10 +/- 59%) or peak systolic velocity (3 +/- 33%). Similar degrees of balloon pump augmentation of distal coronary flow velocity values were observed in five angiographically normal reference arteries in four patients. CONCLUSIONS: These data demonstrate lack of significant flow improvement beyond most critical stenoses with intra-aortic balloon pumping and the unequivocal restoration and intra-aortic balloon pump-mediated augmentation of both proximal and distal coronary blood flow velocities after amelioration of severe coronary obstructions in patients after successful coronary angioplasty.
Aged↗
Chronic hypoxic pulmonary hypertension. Is thrombin involved?
Thrombin contracts vascular smooth muscle and stimulates its proliferation. Using a specific thrombin inhibitor, hirudin, we studied whether thrombin contributes to the pulmonary vasoconstriction and vascular proliferation that occurs in pulmonary hypertension. Hirudin was infused intravenously (0.2 mg/h/kg) by minipumps in nine rats during a 3-wk exposure to hypobaric hypoxia (HH). Vehicle (normal saline) was infused in eight hypoxic control (HC) and seven normoxic control (NC) rats. Sufficient hirudin delivery was confirmed by a failure of undiluted plasma from HH, but not from NC and HC, to clot in response to thrombin. When the plasma samples were diluted 1:10, the thrombin time was significantly prolonged in HH when compared with that in both NC and HC. Although hirudin slightly reduced mean pulmonary arterial pressure in open-chest rats, there was no significant difference between the hypoxic groups in total pulmonary resistance, right ventricle weight, morphologic remodeling of lung vessels, or the perfusion pressure-flow relationship in isolated lungs. Vasoconstrictor responses of isolated lungs to angiotensin II and acute hypoxic challenges were not affected by hirudin treatment. We conclude that hirudin, in a dose sufficient to reduce thrombin's catalytic effect on fibrinogen, does not significantly prevent the development of chronic hypoxic pulmonary hypertension.
Animals↗
Long-acting angiotensin-converting enzyme inhibition: once-daily lisinopril versus twice-daily captopril in mild-to-moderate heart failure.
Once-daily lisinopril (5-20 mg) was compared with twice-daily captopril (12.5-50 mg) in a double-blind, randomized, parallel-group study of angiotensin-converting enzyme (ACE) inhibition conducted in 31 centers for 12 weeks in patients with heart failure (New York Heart Association class II-III) who were currently receiving digitalis and/or diuretics. The drugs were compared with regard to their effects on exercise duration, measured with bicycle ergometry, and on ectopic activity, measured using Holter monitoring. Both drugs significantly increased exercise duration after both 6 and 12 weeks of randomized treatment. Neither ACE inhibitor had any significant impact on the hourly rate of either ventricular ectopic counts or couplets, nor was there any difference between treatments with regard to the proportions of patients in whom ventricular ectopic counts were reduced. Both drugs were well tolerated, with no differences observed between treatments. Potassium, urea, and creatinine levels remained stable for both treatments throughout the study.
Adult↗
[Cardiac function and the skin microcirculation in acromegaly].
The microcirculation was measured by nail-fold capillary video microscopy in 21 patients (12 men, 9 women; mean age 54.7 [29-74] years) with acromegaly. Levels of growth hormone (12.0-71.7 microU/ml) and of somatomedin C (2.4-10.5 IU/ml) were elevated in 10 patients, despite preceding treatment. Eleven patients had an increase in myocardial thickness and nine had impairment of left ventricular function, although only slight in most. Left ventricular hypertrophy was demonstrable even in the absence of hypertension. No patient had evidence of coronary heart disease. Nail-fold capillary video microscopy (capillary density, torque index, reactive hyperaemia, epidermal blood flow) failed to distinguish between successfully treated patients and those with persistently elevated growth hormone concentrations or disease duration of over 5 years. There was no evidence of inadequate capillary blood flow as a cause of abnormal function in hypertrophied organs.
Acromegaly↗
Management of a complicated pericardiocentesis.
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Biopsy, Needle↗
Interpretation of cardiac pathophysiology from pressure waveform analysis: coronary hemodynamics, Part III: Coronary hyperemia.
Basal patterns (systolic/diastolic components) of coronary flow velocity as previously described are generally maintained during hyperemia and can be easily recorded in the catheterization laboratory during pharmacologic stimulation. The interpretation of the clinical significance of coronary vasodilatory reserve may be complicated by both coronary and myocardial diseases. Distal coronary artery hyperemic responses measured with ultrasound Doppler-tipped guidewires will provide new information on traditional observations of coronary physiology in humans.
Adenosine↗
The usefulness of a tracking catheter in complex coronary angioplasty.
Complex lesion angioplasty, such as chronic total occlusions, coronary vessels with right angle take-offs, tortuous vessels, and tortuous internal mammary artery or saphenous vein grafts is a continuing challenge. The complex problems have been successfully managed with novel guiding catheter shapes and ultralow profile balloons. However, on occasion steerable guidewire placement remains extremely difficult, despite significantly improved means of intracoronary manipulations.
Aged↗
Interpretation of cardiac pathophysiology from pressure waveform analysis: cardiac arrhythmias.
Various arrhythmias can produce distorted pressure waveforms, which may be confused with benign physiologic events. Delay in the management of serious arrhythmias can be avoided by vigilant monitoring of systemic pressures.
Arrhythmias, Cardiac↗
Interpretation of cardiac pathophysiology by waveform analysis: adult congenital anomalies.
Congenital anomalies are unusual in adults, but characteristic hemodynamic data facilitate precise diagnoses. A complete evaluation, including assessment for intracardiac shunts, is usually indicated in patients prior to major surgical procedures or electrophysiologic interventions.
Adult↗
The effects of epicardial coronary spasm on intracoronary flow velocity and pressure gradient in a patient after cardiac transplantation.
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Blood Flow Velocity↗
[Excimer laser coronary angioplasty after primary unsuccessful PTCA].
Excimer laser coronary angioplasty is a new technique for ablation of coronary stenosis, however, the indications for its application are still controversial. We describe two male patients, 60 and 65 years old, who underwent unsuccessful balloon PTCA with a short, concentric and calcified coronary stenosis, although balloon inflation pressure was increased to a maximum in both cases. Excimer laser angioplasty following the failed procedures showed no evidence for tissue ablation angiographically, but a repeat attempt with balloon angioplasty was successful in both cases. Thus, laser angioplasty may be considered as an adjunct technique to balloon angioplasty after a failed PTCA in resistant, non-inflatable lesions.
Aged↗
Treatment of unstable angina pectoris (European experience).
Unstable angina pectoris is used to describe accelerated angina, new onset of angina, or prolonged angina. The natural history of the angina varies according to clinical presentation. The 1-year mortality rate ranges from 2% to nearly 40%. Specific therapy includes nitrates, beta-adrenergic blockers, and/or calcium antagonists as well as antithrombotic therapy in the form of aspirin. Patients with severe angina at rest and ST- and T-wave changes should be admitted to a coronary care unit where full-dose heparin is administered. Coronary angiography should be performed in individuals who fail to respond to the conventional therapy in order to evaluate other therapeutic options, including percutaneous transluminal coronary angioplasty (PTCA) and coronary bypass surgery. In some cases, especially in patients with intracoronary thrombus, thrombolytic therapy may be beneficial.
Angina, Unstable↗
Molecular cloning, characterization and expression of cDNA for rabbit brain tissue factor.
Tissue factor (TF) is a membrane anchored glycoprotein that initiates blood coagulation by forming a complex with circulating factor VII or VIIa. TF has been identified in atherosclerotic plaques and may possibly trigger thrombosis after spontaneous plaque rupture as seen in acute myocardial infarction or angioplasty. We have previously developed an atherosclerotic rabbit model for study of the acute and chronic outcomes following angioplasty. As a first step in developing inhibitors of TF, we have isolated and characterized a rabbit cDNA coding for the mature TF. The sequence comparison of rabbit TF cDNA with those of human and mouse TFs show considerable similarity at both the nucleotide and amino acid levels. The TF cDNA when expressed in E. coli demonstrates a procoagulant activity comparable to that of native rabbit brain TF. The TF activity can be blocked by a polyclonal antibody against rabbit TF.
Animals↗
Amniotic fluid contains tissue factor, a potent initiator of coagulation.
A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic initiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue factor antigen and tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually all of the coagulant potential of amniotic fluid. Amniotic tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of optimal phospholipid content, displayed nearly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical configuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor procoagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functionally active tissue factor in amniotic fluid account for the coagulation changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism.
Amnion↗
A polypeptide factor produced by fibrosarcoma cells that induces endothelial tissue factor and enhances the procoagulant response to tumor necrosis factor/cachectin.
Intravascular clot formation, localized to the neoplasm, is an early component of the vascular response to tumor necrosis factor (TNF)/cachectin. Fibrin is closely associated with the endothelial cell surface, and multiple microthromboses lead to reduced blood flow in the tumor. We have identified a tumor-derived mediator which enhances endothelial procoagulant activity and the cellular response to TNF using cultured cells derived from a murine methylcholanthrene A (meth A)-induced fibrosarcoma as a model system. A heat-stable protease K-sensitive polypeptide, Mr approximately 44,000 on nonreduced sodium dodecyl sulfate-polyacrylamide gel electrophoresis (Mr approximately 56,000 reduced), was purified approximately 500,000-fold from serum-free culture supernatants of meth A cells by sequential Q-Sepharose, Mono S, reversed phase, and preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Based on immunologic criteria, biologic activity, and other molecular properties, meth A factor appears to be distinct from other cytokines and growth factors. Purified meth A factor induced transcription of the tissue factor gene and expression of procoagulant activity by cultured human endothelium (half-maximal effect for the latter at approximately 6-8 pM). Furthermore, co-incubation of endothelium with meth A factor together with TNF enhanced induction of tissue factor in a more than additive manner. These data indicate that certain tumors elaborate an apparently unique molecule which can alter hemostatic properties of the vessel wall, potentially modulating reactivity of the tumor vasculature to host response mediators.
Animals↗
[Coincidence of hypertensive fundus changes and regulatory disorders of peripheral microcirculation. II--Skeletal muscles].
In patients with hypertensive fundus changes considerable morphologic changes of the entire vascular system may be assumed. In the present study, the effects of these processes on the partial oxygen pressure of the skeletal musculature were investigated in 62 patients via a macro puncture electrode placed in the tibial muscle. The extent of fundus changes and the reduction in muscular partial oxygen pressure were found to be correlated. With advancing stages of fundus changes, blood flow measured in the common carotid artery decreased. Vascular changes which are clearly recognizable in the hypertensive fundus thus appear to be accompanied by a deterioration in partial oxygen pressure in muscular tissue and restriction of flow in the macrocirculation.
Aged↗
Expression of tissue factor procoagulant activity: regulation by cytosolic calcium.
Intact bovine fibroblasts, pericytes, and kidney cells manifested significantly less tissue factor procoagulant activity than their disrupted counterparts. Addition of calcium ionophore A23187 rapidly and reversibly enhanced the cell-surface expression of tissue factor in intact cells up to the level achieved by disruption. Inhibitors of calmodulin blocked the ionophore-dependent enhancement of procoagulant activity. Similar kinetic parameters were obtained for factor X hydrolysis by tissue factor-factor VIIa on unperturbed pericytes and phosphatidylcholine vesicles. Increase in Vmax and decrease in apparent Km for this reaction were seen after either disruption or ionophore stimulation of the pericytes. Addition of phosphatidylserine to the reconstituted phospholipid vesicles also increased the Vmax and decreased the apparent Km for factor X hydrolysis. These data agree with the hypothesis that the expression of tissue factor procoagulant activity on cell surfaces is modulated by calcium-mediated changes in the asymmetric distribution of phosphatidylserine in plasma membrane.
Animals↗