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Biomedical subjects

J B Lakier

Publications and source records attributed to J B Lakier.

At least 19 recordsLinked to original sources
PubMed2000

Successful management of coronary artery perforation with helical platinum microcoil embolization.

A case of small coronary artery perforation during coronary intervention is presented. Continued leakage occurred despite prolonged intracoronary balloon inflation, in part probably related to the use of glycoprotein (GP) IIB/IIIA inhibitors. It was successfully managed by microcoil embolization without any sequel, helping avoid surgery in a high-risk patient. Cathet. Cardiovasc. Intervent. 51:320-322, 2000.

Aged↗
PubMed1996

Bronchial arteriovenous malformation in a child with hemoptysis. A case report.

Pulmonary arteriovenous (AV) malformations occur sporadically and in the pediatric population are most commonly associated with hereditary hemorrhagic telangiectasia. Hemoptysis is an infrequent presentation in this age group. Pulmonary angiography is considered to be the definitive diagnostic modality. The authors describe an otherwise healthy eleven-year- old girl who presented with massive hemoptysis secondary to a large bronchial AV malformation unrelated to any congenital anomalies. The pulmonary angiogram appeared normal and the diagnosis was established by digital subtraction aortography. Successful embolotherapy was performed by selective injection of polyvinyl alcohol particles into the culprit bronchial artery.

Arteriovenous Malformations↗
PubMed1995

Inadvertent malposition of a transvenous-inserted pacing lead in the left ventricular chamber.

In conclusion, we propose the following approach to prevent and manage lead malposition in the left ventricle: A 12-lead electrocardiogram in the paced mode and an anterior and lateral chest view should be thoroughly inspected shortly after pacemaker implantation. A definitive diagnosis of malposition can be established with these tests. Development of any neurologic symptoms should be attributed to the malpositioned lead until proved otherwise. In such patients, serious consideration should be given to transcatheter or surgical lead extraction after a period of anticoagulation. If this is not possible, chronic anticoagulation with warfarin must be initiated, achieving an international normalized ratio of > or = 2.5. Antiplatelet therapy alone may not confer adequate protection against future cerebral events. Furthermore, most patients with neurologic manifestations do not have echocardiographic evidence of thrombus on the lead. Conversely, presence of thrombus is highly associated with neurologic symptoms. Any intraarterial lead must be removed due to inevitable complications. Patients who have remained completely asymptomatic for > or = 3 years may be followed carefully with no therapy. For asymptomatic patients diagnosed before this time period, we recommend empiric therapy with antiplatelet agents or low-dose warfarin (international normalized ratio 1.5-2) with careful observation for symptoms.

Cardiac Pacing, Artificial↗
PubMed1995

Myocardial infarction with an initially normal electrocardiogram--angiographic findings.

To analyze the paradox of acute myocardial infarction (AMI) with an initially normal electrocardiogram (ECG), we reviewed the records of 732 patients discharged with a final diagnosis of AMI over a 2-year period. Twenty-one patient were identified whose initial ECG was normal and who underwent coronary arteriography during the index hospitalization. According to the ECG evolution, three distinct groups were identified: Group 1: those who subsequently developed ST elevation or Q waves (n = 7), Group 2: those who developed ST depression or T-wave inversion (n = 8), and Group 3: those whose ECG remained normal ( n = 6). Peak creatine kinase (CK), timing of the first ECG change, life-threatening complications, and location of the infarct-related coronary lesion were recorded. Infarct-related coronary lesions were also classified into those in a major coronary trunk versus those in secondary branches. The incidence of AMI with a normal ECG was 3.7%. There was no difference in the frequency of coronary artery involvement in the groups studied: left anterior descending (33%), right coronary artery (38%), and circumflex (28%). All ECG changes developed within the first 48 h of hospitalization; 17 +/- 15 in Group 1, and 24 +/- 12 h in Group 2. All six patients who had a persistently normal ECG (Group 3) had lesions in branch vessels (p < 0.05 when compared with Group 1 plus Group 2). Patients who developed ST elevation or Q waves (Group 1) always had a major artery trunk involved (p < 0.05 when compared with Group 2 plus Group 3). Patients in Group 3 had less myocardial damage and fewer complications compared with the other two groups. Myocardial infarction with an initial normal ECG is uncommon and may result from involvement of any of the three coronary arteries. Electrocardiographic evolution usually occurs within the first 48 h of hospitalization. Patients whose ECGs remain normal appear to have culprit lesions in coronary branches, smaller infarctions, and fewer in-hospital complications.

Coronary Angiography↗
PubMed1994

Left heart pacing and cardioembolic stroke.

Three patients with inadvertently positioned left heart pacemaker leads were admitted for neurological symptoms consistent with embolic stroke. In one of them, the pacemaker lead crossed the interatrial septum, the mitral valve, and entered the left ventricle. In another it was erroneously placed through the subclavian artery, across the aortic valve, and into the left ventricular chamber. In the third patient, the right ventricular lead of a DDD pacemaker was placed in the coronary sinus and the right atrial lead crossed the interatrial septum, and intermittently entered the left ventricular cavity. Once anticoagulation was initiated, symptoms resolved; they recurred when the level of anticoagulation dropped leading to a major stroke in one of the patients. Two of the patients were on aspirin at the onset of symptoms. We believe that every approach must be considered to remove the malpositioned lead. Otherwise, full dose anticoagulation must be initiated since antiplatelet therapy alone does not confer adequate protection against stroke.

Aged↗
PubMed1992

Smoking and cardiovascular disease.

Cigarette smoking is the most preventable cause of cardiovascular morbidity and mortality. Smoking has been associated with a two-to fourfold increased risk of coronary heart disease, a greater than 70% excess rate of death from coronary heart disease, and an elevated risk of sudden death. These risks are compounded in the presence of hypertension, hypercholesterolemia, glucose intolerance, and diabetes, all of which exhibit a synergistic effect with smoking. The relationship between smoking and the risk of peripheral vascular disease has also been well documented. Smokers account for approximately 70% of patients with atherosclerosis obliterans and virtually all those with thromboangiitis obliterans. An association between smoking and cerebrovascular disease remains a matter of debate, although a higher risk of stoke and stroke-related mortality has been observed in smokers than in nonsmokers. Smoking has also been implicated in the development of cor pulmonale, but a direct association with congestive heart failure has not been established. Nicotine and carbon monoxide appear to play major roles in the cardiovascular effects of smoking. Both components adversely alter the myocardial oxygen supply/demand ratio and have been shown to produce endothelial injury, leading to the development of atherosclerotic plaque. Adverse effects on the lipid profile have been noted as well, but the relationship between these changes and the risk of cardiovascular disease remains to be confirmed. Notably, smoking cessation results in a dramatic reduction in the risk of mortality from both coronary heart disease and stroke. In light of the fact that the incidence of smoking has declined primarily among educated sectors of the U.S. population, future efforts must focus on providing effective education, including smoking cessation techniques, to the less-educated groups.

Adult↗
PubMed1989

Comparative hemodynamic and neurohormonal effects of intravenous captopril and digoxin and their combinations in patients with severe heart failure.

The effects of intravenous captopril and intravenous digoxin given separately and in combination on rest and exercise hemodynamics were studied in 16 patients with severe heart failure and sinus rhythm. When given separately, both captopril and digoxin decreased the pulmonary capillary wedge pressure by, respectively, 24% (p = 0.003) and 34% (p = 0.004) and systemic vascular resistance by 23% (p = 0.09) and 20% (p = 0.03). Only digoxin increased cardiac index by 23% (p = 0.03) and stroke work index by 52% (p = 0.01). During maximal exercise, captopril alone decreased systemic vascular resistance by 28% (p = 0.0002) and increased cardiac index by 33% (p = 0.02). Digoxin alone decreased pulmonary capillary wedge pressure by 11% (p = 0.04) and increased stroke work index by 44% (p = 0.01). The combination of captopril and digoxin resulted in a decrease in pulmonary capillary wedge pressure and systemic vascular resistance and an increase in cardiac index and stroke work index both at rest and during exercise that was greater than values observed with either drug given alone. Cardiac index response to the combination of captopril and digoxin correlated with baseline serum aldosterone concentration (r = 0.81, p less than 0.001) and plasma renin activity (r = 0.74, p less than 0.0002). A significant decrease in norepinephrine concentration was noted after digoxin was administered alone or added to captopril. These findings demonstrate that in patients with severe heart failure, the acute administration of captopril and digoxin has an independent salutary hemodynamic effect. The combination of these agents, however, has an adjunctive effect on cardiac function at rest and during exercise.

Adult↗
PubMed1988

Minnesota ALG. Safe and effective immunosuppression for cardiac transplantation.

Fifty-six patients undergoing orthotopic cardiac transplantation were given Minnesota ALG prophylactically or therapeutically for acute cardiac rejection. During a follow-up period of 0-28 months (mean follow-up period, 11.9 months), the actuarial survival for the entire group was 96% and 86% at 30 days and 1 year, respectively. Actuarial freedom from rejection was 60% and 28% at 30 days and 1 year, respectively. All but seven rejection episodes responded to initial steroid pulses or a modification of a maintenance cyclosporine and azathioprine regimen. The seven failures were rescued with further Minnesota ALG therapy. Few serious hematologic or allergic reactions to Minnesota ALG were observed, and no new malignancies occurred during the follow-up period. We conclude that Minnesota ALG is safe and effective in cardiac transplantation.

Coronary Disease↗
PubMed1988

Prevention of early postoperative renal dysfunction in cardiac transplantation.

Fifty six patients undergoing cardiac transplantation were immunosuppressed with a multi-drug induction regimen in which Cs administration was delayed postoperatively until satisfactory hemodynamics and renal function were achieved. The advantage of this approach is the absence of acute renal dysfunction in the early postoperative period. This immunosuppressive regimen was well tolerated and without significant detrimental effects on patient survival, graft rejection, or infection.

Antilymphocyte Serum↗
PubMed1987

Doppler and echocardiographic features of normal and dysfunctioning bioprosthetic valves.

Echocardiographic and Doppler studies were performed on 183 clinically normal and 58 severely dysfunctioning bioprosthetic mitral, aortic and tricuspid valves. The valve dysfunction resulted from spontaneous cusp degeneration in 49 instances and from paravalvular regurgitation in 9. The pulsed Doppler study demonstrated regurgitant flow in 36 (92%) of 39 regurgitant valves and 8 (90%) of 9 paravalvular regurgitant valves. Diagnostic echocardiographic features were present in only 51 and 10% of the patients, respectively. Although the Doppler regurgitant jet was peripheral in seven of the nine patients with paravalvular regurgitation, it was not possible to differentiate these patients from those who had valve degeneration and cusp tear at the periphery of the valve ring. Eight patients presented with a musical holosystolic murmur of mitral insufficiency. In all eight there was a characteristic honking intonation on the audio signal and a striated shuddering appearance on the video Doppler signal. Ten stenotic mitral bioprosthetic valves (less than or equal to 1.1 cm2 valve orifice) were identified by Doppler study. Diagnostic echocardiographic features were present in only two of these patients. The Doppler-derived valve orifice dimension correlated well (r = 0.83) with cardiac catheterization values. Fourteen asymptomatic or minimally symptomatic patients had echocardiographically thickened mitral cusps (greater than or equal to 3 mm). These patients had a significantly (p less than 0.0001) smaller valve area as compared with normal control valves, and during 4 to 24 months of follow-up, five of these patients developed severe valve regurgitation or stenosis. Doppler ultrasound is more sensitive than echocardiography in diagnosing bioprosthetic valve stenosis and regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

In vivo evaluation of intracellular pH and high-energy phosphate metabolites during regional myocardial ischemia in cats using 31P nuclear magnetic resonance.

Phosphorus-31 nuclear magnetic resonance spectroscopy (31P NMR) was used to assess the temporal changes of high-energy phosphate metabolites in the region of acute myocardial ischemia of open-chest cats. Eight anesthetized cats were studied following ligation of the left anterior descending coronary artery. Creatine phosphate showed a 79 +/- 16% (mean +/- SD) reduction by 4 min after the onset of ischemia. Prominent qualitative reductions of the spectral peak of creatine phosphate occurred by 40 s after ischemia. Adenosine triphosphate measured under the beta spectral peak (beta-ATP) decreased 37 +/- 9% by 20-25 min after ligation of the left anterior descending coronary artery. These reductions developed more slowly and were of smaller magnitude than those of creatine phosphate. Intracellular pH decreased from 7.39 +/- 0.07 to 7.13 +/- 0.09 units by 40 s after ischemia. By 30 min, pH decreased to 6.07 +/- 0.40 units. The study shows, therefore, the temporal changes of high-energy phosphate metabolites during ischemia in localized regions of the myocardium of open-chest animals.

Adenosine Triphosphate↗