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Biomedical subjects

C R Conti

Publications and source records attributed to C R Conti.

At least 145 records · Page 8Linked to original sources
PubMed1994

Atrial fibrillation, transesophageal echo, electrical cardioversion, and anticoagulation.

Although successful electrical cardioversion is accomplished in most cases without any evidence of embolic stroke, a few patients have experienced this catastrophe. The current thinking is that when electrical energy is applied to the chest wall, the atrium, although it returns to sinus rhythm, is stunned. It is not known how long this stunning lasts in the individual patient nor whether high energy produces stunning and low energy does not. Nor is it known whether chemical conversion of atrial fibrillation to sinus rhythm affects the atrium in the same way. However, the atrium seems to recover more quickly in patients with a short duration of atrial fibrillation and these patients may not require the usual four weeks of postcardioversion anticoagulation. Based on what we know, or more precisely what we don't know, it seems reasonable to ensure that every patient with atrial fibrillation is anticoagulated during and after DC cardioversion to sinus rhythm. Of course, this is easy to do with intravenous heparin, but that requires hospitalization. Perhaps subcutaneous heparin in high doses would suffice until the patient can be anticoagulated with coumadin. From the research perspective it might be interesting to perform serial echo/Doppler studies on these patients to identify when the individual patient's atrial function returns to normal. This might provide a clinical rationale for discontinuing anticoagulation. Comparing the time to return of normal atrial function (as measured by Doppler echo) between patients undergoing pharmacologic cardioversion versus electrical cardioversion and studying the relationship of the amount of electrical energy required for cardioversion versus the duration of stunning would be clinical research projects of interest to clinicians.

Anticoagulants↗
PubMed1994

Constrictor and dilator responses to intracoronary acetylcholine in adjacent segments of the same coronary artery in patients with coronary artery disease. Endothelial function revisited.

BACKGROUND: In patients with angiographically detectable atherosclerosis or in those with risk factors for coronary artery disease, intracoronary acetylcholine causes coronary constriction instead of endothelium-derived relaxing factor-mediated dilation. Therefore, it has been hypothesized that diffuse endothelial dysfunction precedes development of coronary atherosclerosis. We tested this hypothesis in a systematic investigation of the effects of ascending doses of acetylcholine on the diameters of nonstenotic segments of the left coronary artery in patients with advanced atherosclerosis and coronary risk factors. METHODS AND RESULTS: Effects of intracoronary infusion of acetylcholine (10(-6) to 10(-4) mol/L) on diameters of proximal, middle, and distal nonstenotic segments of the left coronary artery were studied in 28 consecutive patients with chronic stable angina, positive exercise tests, and angiographic evidence of obstructive atherosclerosis (> or = 50% reduction in lumen diameter in at least one vessel). Two patterns of response to the maximal acetylcholine dose (10(-4) mol/L) were observed. In 21 patients (group 1), only constriction was observed in all left anterior descending and circumflex artery segments studied (16 +/- 3%, 19 +/- 4%, and 23 +/- 4%, respectively; P < .01 compared with control). In 7 other patients (group 2), both constriction and dilation were observed in adjacent segments of the same vessel; maximal acetylcholine dose caused constriction in 14 left anterior descending artery segments from a control diameter of 1.94 +/- 0.19 to 1.33 +/- 0.26 mm (37% reduction, P < .01) and dilation in 16 other segments from 1.63 +/- 0.22 to 1.93 +/- 0.21 mm (25% increase, P < .01). In the circumflex artery, this dose caused constriction in 16 segments from a control diameter of 1.88 +/- 0.14 to 1.33 +/- 0.17 mm (31% reduction, P < .01) and dilation in 12 segments from 1.37 +/- 0.12 to 1.71 +/- 0.09 mm (34% increase, P < .01). CONCLUSIONS: In 25% of patients studied with advanced angiographic coronary atherosclerosis and coronary risk factors, coronary segments with acetylcholine-inducible dilatation are present. In these patients, the endothelium is not diffusely dysfunctional as currently believed but rather shows marked segmental heterogeneity in the response to acetylcholine reflecting degrees of endothelial dysfunction.

Acetylcholine↗
PubMed1993

Unstable angina: relationship of clinical presentation, coronary artery pathology, and clinical outcome.

Patients with unstable angina are heterogeneous with respect to presentation, coronary artery morphology, and clinical outcome. Subclassification of these patients based on clinical history has been proposed as a means of identifying individuals at increased cardiac risk. We applied such a classification system to 129 patients discharged from a coronary care unit with a diagnosis of acute myocardial ischemia. Patients were then assessed for cardiac events (recurrent angina requiring revascularization, myocardial infarction, death) 12 months following hospital discharge. Patients were classified as recent onset unstable angina preinfarction (n = 42), crescendo unstable angina preinfarction (n = 48), and unstable angina postinfarction (n = 39). Within each of these groups, the patients were further subclassified based on the occurrence of angina on effort, at rest, or both. No attempt was made to subset patients taking anti-ischemic drugs at the time of clinical presentation to the physician. Coronary angiographic pathology (morphology and number of vessels involved) was similar in the subgroups, but coronary artery thrombus was statistically more likely to be found in patients with crescendo rest angina preinfarction or with frequent anginal episodes at rest postinfarction. Mortality was significantly higher for patients with unstable angina postinfarction (7.7%) than preinfarction (1.1%). No statistical differences were noted between the subgroups with respect to the occurrence of myocardial infarction or recurrent unstable angina requiring revascularization. These data suggest that subclassification of unstable angina patients based on clinical characteristics at presentation is not useful to predict subsequent myocardial infarction or recurrent angina requiring revascularization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Transseptal left heart catheterization for radiofrequency ablation of accessory pathways.

In summary, I think it is important to state that transseptal left heart catheterization is a safe procedure when the operator pays meticulous attention to detail. Potential complications can be avoided if the operator: (1) heparinizes the sheath prior to catheterization, (2) fully heparinizes the patient when the catheter and sheath are across the septum, and (3) remembers that the left atrium in these patients is quite small and can be perforated easily by the tapered tip of the transseptal catheter. Transesophageal cardiac ultrasound makes this latter point very clear to anyone doing this procedure.

Arrhythmias, Cardiac↗
PubMed1993

Heart failure: drug therapy in the nineties and beyond.

The lesson learned from recent advances in the understanding of congestive heart failure is that it is too complex a process to be managed in a simple fashion. At present, incremental improvement such as that provided by ACE inhibitors, and now possibly by new agents such as flosequinan, are what we have to offer our patients, short of transplantation, to control symptoms and increase exercise tolerance. No one knows what the future holds for these patients, but one can hope that the current therapy and those drugs being studied in clinical trials will provide agents that will continue to reduce the morbidity and mortality associated with current therapies. However, only so much can be done with drugs in the failing heart, and research must continue in the area of cardiac transplantation as well as in the area of totally implantable ventricular assist devices.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Stroke and atrial fibrillation: to anticoagulate or not.

After reviewing these published studies, I think one can conclude that in the patient population with chronic and/or paroxysmal atrial fibrillation, warfarin is beneficial and the benefits outweigh the risks. However, it is important to point out that patients at high risk for embolic disease, for example, dilated cardiomyopathy patients, were rarely included in these trials. The five trials mentioned above do not address this patient population. Current opinion is that these individuals should receive anticoagulation despite the lack of objective evidence that anticoagulation is beneficial if the risk of bleeding is not excessive. The five trials also do not address the population of patients categorized as having "lone atrial fibrillation," that is, atrial fibrillation occurring in patients with no structural heart disease. The general consensus in the low embolic risk patient, (i.e., the patient < 60 years of age who has lone atrial fibrillation) is that the risk of anticoagulation is greater than the benefit. My final thought on the subject concerns the risk of pulmonary emboli in this patient population. My guess is that this group of patients is at high risk for small pulmonary emboli, which in many instances may be subclinical--for example, clots too small to result in persistent tachypnea or tachycardia. As far as I can tell, there are no randomized trials on the prevention of pulmonary emboli in patients with chronic or paroxysmal atrial fibrillation using anticoagulation or aspirin. I guess the systemic emboli trial data are sufficient to indicate a protective effect on the lungs as well as on the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Risk of cardiac surgery in patients with peripheral vascular disease.

After reading these articles, I think the evidence is convincing that peripheral vascular disease clearly places the patient at a higher risk for coronary bypass surgery than is the case for patients without peripheral vascular disease. However, in some instances coronary bypass surgery must be performed before peripheral vascular surgery is performed. Perhaps the best way to leave it is to indicate that if there is a clear-cut indication for coronary bypass surgery it should be done independent of vascular disease elsewhere, but one must accept the fact that most reports indicate an increased morbidity and mortality. Thus, I would like to make a final point by quoting Gersh: "The protective shield of prior coronary artery bypass surgery [in patients with peripheral vascular disease] . . . has a price."

Coronary Artery Bypass↗
PubMed1993

Vascular events responsible for thrombotic occlusion of a blood vessel.

In summary, the sequence of endothelial plaque disruption, platelet activation, and thrombogenic factors--that is, the balance between the thrombolytic system and the coagulation system--determine which blood vessel will thrombose and which vessel will remain patent. It seems to me that although the soft plaque with the thin cap and lipid core laden with oxidized LDL-activated macrophages is more prone to rupture than the calcified, hard plaque, it is also the plaque that may regress when the patient is treated aggressively with lipid-lowering or antioxidant therapy. In addition, drugs that lower blood pressure and heart rate may also decrease the tendency of the "vulnerable" plaque to rupture by attenuating fatigue failure. Current and future research should be directed at identifying vulnerable plaques in the individual patient, so that measures can be taken to prevent plaque rupture.

Coronary Artery Disease↗