Surgery: light – thermal – and electrical application – Light – thermal – and electrical application – Electrical therapeutic systems
Reexamination Certificate
1999-10-13
2002-10-29
Layno, Carl (Department: 3762)
Surgery: light, thermal, and electrical application
Light, thermal, and electrical application
Electrical therapeutic systems
C607S009000
Reexamination Certificate
active
06473644
ABSTRACT:
BACKGROUND OF THE INVENTION
The present invention relates generally to nerve stimulation, and more particularly to cranial nerve stimulation to stimulate or enhance cardiac capillary growth and cardiac output in heart failure patients.
Heart failure is a cardiac condition or disorder characterized by an abnormal cardiac function—specifically, low cardiac output—that leaves the heart unable to meet the circulatory, oxygen replenishing needs of the body. An estimated 2 million or more individuals in the United States meet the clinical definition of heart failure, making this disorder a major health problem. Although some of the affected individuals are relatively symptom free, those with severe heart failure have very little physical endurance and may be bedridden. Heart rate is one of the major determinants of myocardial oxygen consumption.
It is customary to lower the patient's heart rate as a method of treating heart failure. A lowered heart rate has the effect of improving the oxygen balance in the heart by reducing oxygen demand, while increasing supply through better coronary perfusion, particularly sub-endocardial, during a longer diastolic interval. This scheme is tolerable provided that the working capacity of the individual is not reduced to unacceptably low levels. Because of the complex control system linking heart rate via cardiac output to regulation of blood pressure and peripheral perfusion, most interventions resulting in long term bradycardia involve additional actions on the periphery through direct or indirect neuronal and/or hormonal mechanisms. Physiological bradycardia occurring with exercise training, and pathological bradycardia such as A-V block, are associated with activation of the sympathetic nervous and renin-angiotensin systems and enhanced catecholamine release. One effect of long-term bradycardia common to these situations is myocardial hypertrophy.
With pharmacological methods of inducing bradycardia—for example, by ingestion of beta blockers, calcium channel blockers, or selective bradycardia drugs—it may be difficult to avoid unwanted negative ion inotropy and systemic effects of the drugs, particularly if they are used on a chronic basis. However, even with these side effects, beta blocker therapy is highly beneficial to those patients who can tolerate the side effects. Recently published studies by Carson (
Progress in Cardiovascular Diseases
, Vol 31, No 4, 1999: pp 301-322) reported a 20% reduction in the risk ratio for mortality in patients treated with beta blockers, although patients received little or no improvement in cardiac output.
Brown et al, in an article titled “Long term bradycardia by electrical pacing: a new method for studying heart rate reduction,”
Cardiovascular Research
1994; 28: pp. 1774-1779, demonstrated the benefits of using pacing to lower heart rate in pigs. The researchers used a method of stimulating both the atrial and ventricular chambers of the heart to reduce heart rates from about 130 beats per minute (bpm) to about 85 bpm. The animals were maintained at the lower rate for about six weeks. Autopsies revealed that myocardial capillary was increased by about 20%. No evidence was found of the cardiac hypertrophy associated with pharmacological methods of reducing bradycardia, either on the basis of heart weight or on estimates of myocyte size.
Bilgutay et al., in an article titled “Vagal Tuning,”
J Cardiovas. Surg
. 56(1):71-82 described studies in dogs with right vagal stimulation for treatment of supraventricular arrhythmias, angina pectoris, and heart failure. The experiments involved right vagus nerve stimulation and resulted in a selection of amplitude of 6 to 10 volts, a frequency of 10 pulses per second, and 0.2 msec pulse duration. In all experiments, the coronary flow remained constant. However, the heart rate was decreased 35 to 50 percent. The increase in percentage of coronary flow per heart beat was found to be 75 to 100 per cent. In another experiment, Bilgutay administered Isuprel to induce tachycardia, which increased heart rate from 170 bpm to 240 bpm. He then stimulated the vagus nerve and reduced the heart rate from 240 bpm to 120 bpm. The ventricular and aortic pressures were unchanged by vagus stimulation, whereas the systole and diastole were prolonged. These results indicated the contractility of the heart was increased in this model of tachycardia, while the slower rate was maintained, resulting in an increase in cardiac efficiency due to greater stroke output. Although he discussed the potential benefits of treating a failing heart, none of the experiments involved models of heart failure, nor did he anticipate increased capillary growth.
Feliciano et al, in an article titled “Vagal nerve stimulation during muscarinic and beta-adrenergic blockade causes significant artery dilation,”
Journal of the Autonomic Nervous System
, 68 (1998), pp. 78-88, demonstrated that vagal nerve stimulation in dogs significantly dilates the coronary arteries and significantly increases coronary artery blood flow. Stimulation was performed at frequencies of 10, 15, 20, and 30 Hertz (Hz). In these studies, the muscarinic and beta-adrenergic receptors were blocked with atropine and propranolol.
Heart rate was controlled at normal rates by pacing. Feliciano did not demonstrate artery dilation in normal conditions, without atropine, propranolol and rate stabilization by pacing, nor did he demonstrate an increase in capillary growth.
Vagus stimulation of the left cardiac branch of the vagus nerve to lower ventricular heart rate in the presence of atrial fibrillation is described by Geddes et. al. in U.S. Pat. No. 5,690,681, and the more recently issued U.S. Pat. No. 5,916,239. As disclosed in the '681 patent, a closed loop, variable frequency vagal stimulation apparatus was used to control ventricular rate during atrial fibrillation. The apparatus included means for stimulating a vagal nerve at a stimulation frequency which was varied automatically in response to sensed conditions, and a controller having an output connected to the stimulating means. The latter included means for automatically and continuously adjusting the vagal stimulation frequency as a function of the difference between actual and desired ventricular excitation rates.
The apparatus of the '681 patent was stated to automatically control ventricular rate by vagal stimulation, to minimize pulse deficit during atrial fibrillation. The arterial pulse rate was detected and the ventricular excitation rate and arterial pulse rate were compared. The vagal stimulation frequency was automatically adjusted as a function of the difference between the ventricular excitation rate and the arterial pulse rate.
A number of patents describe various methods of vagus stimulation for the control of ventricular arrhythmias. U.S. Pat. No. 5,203,326 to Collins discloses a pacemaker which detects a cardiac abnormality—a pathologic high rate—and responds with pacing combined with vagus nerve stimulation, to reduce the heart rate from the tachyrhythmia rate to the normal rate. U.S. Pat. No. 5,330,507 to Schwartz describes stimulation of the right or left vagus nerve in response to a ventricular rate exceeding a predetermined threshold characteristic of tachycardia.
European Pat. No. 688577A1 to Holmstrom describes stimulation of the parasympathetic nervous system in the neck in response to detection of a supraventricular arrhythmia. The vagus nerve is a parasympathetic nerve. U.S. Pat. No. 5,700,282 to Zabara describes a process s for monitoring the heart to detect arrhythmias and simultaneous stimulation of the vagus and cardiac sympathetic nerves to stabilize the heart rhythm. U.S. Pat. No. 5,658,318 to Stroetmann describes detecting a state of imminent cardiac arrhythmia from nerve activity signals and administering antiarrhythmia therapy. U.S. Pat. No. 5,522,854 to Ideker describes detection of the ratio of sympathetic to parasympathetic nerve activity and delivering stimulation to afferent nerves u upon detection of a high-risk arrhythmia. None o
Adkins Alan
Barrett Burke
Terry, Jr. Reese S.
Blank Rome Comisky & McCauley LLP
Cyberonics, Inc.
Layno Carl
LandOfFree
Method to enhance cardiac capillary growth in heart failure... does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Method to enhance cardiac capillary growth in heart failure..., we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method to enhance cardiac capillary growth in heart failure... will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-2993202