Unstable angina: Rational approach to management

The successful use of spinal cord stimulation (SCS) in patients with stable angina pectoris refractory to medical management who are poor candidates for percutaneous or surgical angioplasty has been well described [1]. Janfaza et al. [2] recently described a critically ill patient with unstable angina pectoris who was treated with SCS. The patient's condition improved and stabilized, and the patient was discharged from the hospital and survived for at least 6 wk. To the best of our knowledge, there are no other reports of the use of SCS in such critically ill patients. We describe two similar patients treated with SCS but with different outcomes. Case Report 1 A 79-yr-old man was transferred to the cardiology service for treatment of intractable angina pectoris. He had experienced increasingly frequent and severe substernal chest pain, dyspnea, and diaphoresis worsened by mild exertion and mental stress for 8 days before this transfer. His electrocardiogram (EKG) showed new ST-segment depression in leads V3-V6. He was receiving IV heparin, nitroglycerin, and morphine in addition to oral metoprolol and nifedipine at the time of admission. An urgent cardiac catheterization showed severe three-vessel disease in addition to an 80% left main occlusion. The patient had suffered two previous myocardial infarctions and a cerebrovascular accident (CVA), and he had bilateral 100% carotid artery occlusions. He had a medical history of noninsulin-dependent diabetes mellitus, hypertension, severe peripheral vascular disease, and a 4.0-cm abdominal aortic aneurysm. Despite aggressive medical management, the patient continued to have severe and protracted episodes of chest pain at rest. His lesions were not amenable to percutaneous angioplasty, and he declined coronary artery bypass grafting because of the high risk of recurrent CVA. He decided not to be resuscitated or intubated in the event of a sudden decline in his status. On the 10th day after admission, the acute pain service was consulted. After a thorough discussion with the patient and his family regarding the risks, potential benefits, and uncertainty about the efficacy of the procedure under the current circumstances, the patient and his family agreed to a trial of SCS. The patient's heparin was stopped for 4 h, and coagulation variables were determined to be normal. The patient was taken to the operating room, monitored, lightly sedated by an anesthesiologist, and placed in the prone position. Anesthesia was accomplished by local anesthetic infiltration. A 15-gauge Tuohy needle was inserted at the T4-5 interspace. Position was identified and confirmed fluoroscopically throughout the procedure. The epidural space was identified using a loss-of-resistance to air technique. A Pisces Quad-Plus Electrode (Medtronic, Inc., Minneapolis, MN) was inserted into the epidural space and advanced under fluoroscopic guidance until the tip lay at the C7-T1 interspace and approximately 3 mm to the left of midline. A trial paresthesia was found to encompass the entire area of anginal pain. Electrode configuration was 0 = off; 1 = positive, 2 = negative, 3 = off. Pulse width was 300 ms and rate was 50 Hz. The threshold for paresthesia was 1.5 V, and the maximally tolerable paresthesia was 1.9 V. The procedure was well tolerated by the patient. Stimulation was kept constant at 1.6 V; if the patient had an episode of angina, the voltage was increased to 1.9 V until it resolved. The patient's IV medications were discontinued. Oral nitrates and morphine sulfate were used as needed. The patient had fewer and less severe episodes of angina. He was transferred out of the coronary care unit (CCU). Three days after placement of the trial electrode, the patient experienced worsening angina unrelieved by SCS, and he was transferred back to the CCU. IV heparin was resumed. His EKG indicated new ischemic changes, and he had signs and symptoms of congestive heart failure. His chest pain required SCS and IV morphine and nitroglycerin for control. On the fifth day after SCS implantation, the patient died quietly. Case Report 2 An 86-yr-old woman was admitted with a 1-wk history of uncontrolled left shoulder pressure radiating into her left arm and hand. At the time of admission, she was receiving metoprolol, amlodipine, and ticlopidine. She was treated with IV heparin, nitroglycerin, and morphine. The patient had a history of sinus node disease and had a dual-pacing, dual-sensing, dual-mode pacemaker. She had previously suffered a CVA and a myocardial infarction and had undergone percutaneous coronary angioplasty. She had a history of hypertension and peripheral vascular disease. An urgent cardiac catheterization and an attempt at revascularizaton via percutaneous angioplasty resulted in closure of the right coronary artery. The patient's creatinine phosphokinase level was increased, consistent with an acute myocardial infarction. She decided not to be resuscitated or intubated in the even her condition worsened. She was deemed to have a high risk of death and stroke with surgical bypass, and the acute pain service was consulted about the implantation of a SCS device. Informed consent was obtained, and the device was implanted as with the previous patient. Electrode configuration was 0 = off; 1 = positive, 2 = negative, 3 = off. Pulse width was 200 ms and rate was 80 Hz. The threshold was 2 V, and the patient's maximally tolerated voltage was 2.1 V. Paresthesia covered her entire painful area. IV medications were gradually discontinued. The patient had fewer episodes of angina, which were all easily aborted with SCS. Four days after her trial electrode was placed, the patient was returned to the operating room, and an Itrel 2 generator (Medtronic, Inc., Minneapolis, MN) was implanted into the right buttock area. She was transferred out of the CCU. The following evening, she developed palpitations while her SCS device was on at the threshold voltage, and an EKG showed ventricular tachycardia. The patient declined any treatment and subsequently developed left shoulder pain, which was incompletely but adequately relieved with her SCS device increased to 2.1 V. She became unconscious and died approximately 10 min later. Discussion Both of these patients had symptoms of ischemia when their cardiac status deteriorated. This supports the work of other investigators who have shown that SCS does not mask the symptoms of ischemia but improves the function of the heart [3,4]. There is a single report of interference between an unipolar pacemaker and unipolar SCS [5]. The safe use of a dual-pacing, dual-sensing, dual-mode pacemaker in conjunction with quadriploar SCS electrodes has been described [6]. It is unlikely that the arrhythmia observed in our second patient was the result of pacemaker interference, although it is possible. Janfaza et al. [2] reported the six-week survival of a single critically ill patient treated with SCS. Our cases suggest relief of pain but no, or minimal, survival advantage in this critically ill population. Although both patients experienced improvement of their anginal symptoms with SCS, the effect was not sufficient to overcome the severity of their ischemic disease. There is evidence demonstrating pain relief, low morbidity, and improved function of the heart in patients with stable angina treated with SCS [1]. Our patients had unstable angina and were considered terminally ill, with a life expectancy estimated in days to weeks. It may be that SCS is not indicated in endstage unstable angina because of its inability to prolong life, as demonstrated in the patients presented, but this remains undetermined. The precise niche for SCS in the treatment of angina is still being investigated.

Current Evidence For The Use Of Platelet Gpiib/iiia Receptor Inhibitors In Acute Coronary Syndromes

Setting a New Gold Standard

Heparin and Low-Molecular-Weight Heparin Mechanisms of Action, Pharmacokinetics, Dosing, Monitoring, Efficacy, and Safety

The introduction of coronary artery stents into widespread clinical use in the mid-1990s was a significant advance that almost rivals the introduction of balloon angioplasty itself 15 years earlier. It is noteworthy that the success of stents required several paradigm shifts. For example, higher-pressure balloon inflations and slight oversizing were needed to achieve full stent expansion (anathema in balloon angioplasty), and antiplatelet therapies were required rather than anticoagulation, including a reduction and now almost elimination of heparin. Yet, these changes were quickly accomplished. Technical advances in equipment also occurred, and now stenting, quite literally, has become the standard in clinical practice when it can be performed (which is most of the time). One curious and intriguing question that arises with any new device, and stents are no exception, is whether they are needed in all situations where they are being used. Is it possible that balloon angioplasty alone might be sufficient for excellent immediate and long-term benefit, provided the final procedural result is good enough? If one could determine this to be true, then such a strategy would avoid the additional cost of a stent and the problem (or pseudo-problem) of in-stent restenosis. However, a provisional stent strategy raises the further and not inconsiderable question of how to decide when balloon angioplasty results are “good enough.” The limitations of standard angiography notwithstanding, is there anything better than the eyes and minds of experienced angiographers? Additional “objective” measures to assess procedural results have long been sought. A number of investigators have championed intracoronary ultrasound as one approach, whereas others suggest alternative methods. In this issue of Circulation , 2 separate groups report their findings using combined anatomic and functional coronary measures to assess balloon angioplasty results for the purpose of provisional stenting.1 2 These measures are on-line quantitative coronary arteriography …

Percutaneous transluminal angioplasty of saphenous vein grafts for medically refractory unstable angina

Background Atrial fibrillation is the most common arrhythmia in United States, and is associated with atrial fibrosis. Although the cause of atrial fibrosis development is not understood, its etiology is related to cardiac dysfunction, mitral regurgitation (MR), and coronary artery disease. This study focuses on determining the acute effects of myocardial infarction (MI) on left atrial (LA) function. Our hypothesis is that MI may result in changes in left ventricular relaxation, MR, and LA pressure and volume overload, leading to changes in LA geometry and mechanics, which will result in later atrial fibrosis. We studied the changes in LA size, ejection fraction, and the relative contributions of passive and active emptying, comparing controls with post-MI animals. Methods Eleven Yorkshire pigs (average weight 37 ± 7 kg) were studied, including 5 control animals, and 6 pigs imaged one to two weeks after a transmural MI. The MI was induced by percutaneous balloon occlusion of left coronary artery (90 min) followed by reperfusion. All animals were imaged on a 1.5T Siemens scanner (Siemens Healthcare, Erlangen, Germany). A stack of short-axis cine images covering the left atrium were obtained with balanced SSFP, with a 1.3 x 1.3 x 3 mm spatial resolution (no gaps), and 25 frames, breath-holding and retrospective ECG-gating. All image processing was performed in Matlab (v 2014). To measure LA volume through the cardiac cycle, the cine images were segmented using thresholding, and regions of

The haemodynamic status of 8 coarctated and 7 sham-operated beagle puppies was studied by a catheterization technique at rest and during isoproterenol and volume loading at the ages of 7 (I) and 9 (II) months (5 and 7 months after the experimental coarctation). Proximal aortic systolic and pulse pressures were constantly higher in the coarctation group than in the control group (P less than 0.05), and the systolic pressure gradient across the coarctation was always significantly higher in the coarctation group [I at rest mean 45 +/- 5 (SD) vs 5 +/- 4 mmHg, P less than 0.001, and after I isoproterenol infusion 56 +/- 9 vs 10 +/- 6 mmHg, P less than 0.001, and after I dextran infusion 58 +/- 10 vs 8 +/- 7 mmHg, P less than 0.001]. The time constant of exponential isovolumic left ventricular pressure fall after the isoproterenol tests was longer in the coarctation group (I 28 +/- 8 ms and II, 30 +/- 4 ms) than in the control group (I, 21 +/- 2, P less than 0.05 and II, 19 +/- 3 ms, P less than 0.005), indicating impaired relaxation. The tension time index during the volume loading tests increased in the coarctation dogs (I, 4150 +/- 660 and II, 4080 +/- 810 mmHg s min-1) to higher levels than in the control group (I, 3550 +/- 220, II, 2540 +/- 1140 mmHg s min-1, P less than 0.05 both). Cardiac output, left ventricular end diastolic pressure, inotropic parameters and heart rate were similar in both groups during the infusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Isovolumetric relaxation flow in patients with ischemic heart disease

Heparin is an effective, widely used treatment for unstable angina. Among patients enrolled in a double-blind, randomized, placebo-controlled trial comparing intravenous heparin, aspirin, both treatments, and neither during the acute phase of unstable angina, we encountered patients in whom unstable angina was reactivated after heparin was discontinued. The study population included 403 of the original 479 patients in the trial who had completed six days of blinded therapy without refractory angina or myocardial infarction. After the discontinuation of therapy, clinical events, including reactivation of unstable angina and myocardial infarction occurring within 96 hours after hospitalization, were closely monitored. Early reactivation occurred in 14 of the 107 patients who received heparin alone, as compared with only 5 patients in each of the other three study groups (P less than 0.01). These reactivations required urgent intervention (thrombolysis, angioplasty, or coronary-bypass surgery) in 11 patients treated with heparin alone, but in only 2 patients in the other groups combined (P less than 0.01). Four of the six patients who had a myocardial infarction during a reactivation of their disease were in the heparin group. Reactivations in this group occurred in a cluster a mean (+/- SD) of 9.5 +/- 5 hours after the discontinuation of the study drug but were randomly distributed over the initial 96 hours in the other three groups. Although heparin is beneficial in treating unstable angina, the disease process may be reactivated within hours of the discontinuation of this drug. Concomitant therapy with aspirin may prevent this withdrawal phenomenon.

Background: Chest pain or discomfort caused by acute coronary syndrome (ACS) or angina has a potentially poor prognosis, emphasizing the importance of prompt and accurate diagnosis. To evaluate a clinic set up specifically to assess patients with recent onset chest pain, particularly those presenting with a normal resting electrocargram.Method: The cross-sectional study was carried out from September 2016 to August 2017 in cardiology department of Shaheed Suhrawardy Medical College hospital, Sher-E-Bangla Nagar, Dhaka. Total 1000 consecutive patients with recent onset chest pain were evaluated within 24 hours of general practitioner referral, to find out the clinical diagnosis and management.Results: Total 1000 patients (535 men and 465women, mean age 51.5±11.4 years with range from 32 to 70 years) were assessed over 12 months. Most of the patients 844 (84.4%) had symptoms in duration of ≤30 days. Majority 433 (43.3%) patients had peptic ulcer disease (PUD), 317 (31.7%) patients had chronic stable angina (CSA), 94 (9.4%) had unstable angina (UA), 92 (9.2%) had anxiety neurosis (AN) and 64 (6.4%) had myocardial infarction (MI). Regarding outcome of the patients 525 (52.5%) [PUD: 433+ AN: 91] patients considered to have noncardiac pain and referred to medicine outpatient department (OPD) without further follow up. In a further 317 patients (31.7%, CSA) arrangements were made for outpatient review. Ninety four patients (9.4%, UA) were referred to National Institute of Cardiovascular diseases (NICVD) for admission out of them 61 patients were admitted for medical treatment & 33 patients were discharged from emergency department whose troponin-I were negative. Remaining 64 (6.4%) acute MI patients were admitted into Coronary Care Unit (CCU) of NICVD, out of them 41 patients received streptokinase injection, 23 patients received Enoxaparin injection, after conservative treatment all patients were advised to do coronary angiography within 3 to 4 weeks. Among these 43 patients underwent coronary angiography within 4 weeks, 23 patients had coronary angioplasty, eleven patients had coronary bypass surgery and nine patients refused any intervention and discharged with medicine.Conclusion: This experience highlights the inadequacy of a routine electrocardiogram reporting service in patients with recent onset of chest pain. Clinical diagnosis found were peptic ulcer disease (PUD), chronic stable angina (CSA), unstable angina (UA), anxiety neurosis and myocardial infarction (MI). Regarding outcome of the patients were coronary angiography followed by coronary angioplasty, coronary artery bypass surgery, discharged with medicine and referred to out patients department of medicine unit.J Shaheed Suhrawardy Med Coll, December 2017, Vol.9(2); 65-68

Blood loss was studied in 200 patients during and after coronary artery bypass surgery. Half of the patients were receiving dalteparin/heparin treatment for unstable angina and taking acetylsalicylic acid (ASA) 75 mg/d. One stable and four unstable patients were re-explored because of postoperative bleeding (p = 0.17). Median blood loss was 500 ml (range 100-1700 ml) during the operation and 600 ml (range 200-3400 ml) after the operation. Regression analysis showed a correlation between less postoperative bleeding and female gender and larger body mass index. In our subset of patients this correlation was not predicted from unstable angina, ASA treatment, use of aprotinin, age or cardiopulmonary bypass time. The unstable patients had lower haemoglobin levels before the operation and received blood transfusions postoperatively more frequently. A total of 101 patients were given a blood transfusion. Our findings indicate that ASA can be safely continued until the day of isolated coronary artery bypass surgery.

The aim of this study was to determine the plasma and pericardial levels of endothelin-1 (ET-1) and its precursor big endothelin-1 (Big ET-1) in patients with unstable and stable angina prior to and following coronary bypass surgery. To further investigate the content of ET-1, tissue levels were studied in the internal mammary artery (IMA) in patients with stable and unstable angina pectoris. Finally, the difference in reactivity of the IMA to ET-1 and Big ET-1 in stable and unstable patients was evaluated. Plasma and pericardial levels of ET-1 and Big ET-1 were determined with radioimmunoassay in 81 patients (33 unstable) immediately before coronary bypass surgery, and at 6, 14, 40 and 64 h following the procedure. Specimens of the distal IMA from 12 patients (six unstable) were collected at the beginning of surgery for determination of tissue levels of ET-1. Additionally, distal internal mammary arteries were obtained from another 24 patients (12 unstable). These vessels were mounted in organ baths for functional studies on vascular reactivity to ET-1 and Big ET-1. The peripheral plasma levels of ET-1 in unstable patients were significantly lower in patients with unstable angina compared with patients with stable angina pectoris at all points of measurement. The levels of Big ET-1 were significantly higher pre-operatively in the unstable group, but decreased to similar levels to those of stable patients following coronary bypass grafting. There was no difference in ET-1 tissue content in the IMA between the patients. ET-1 and Big ET-1 caused an endothelin(A) (ET(A))-receptor blocker sensitive, concentration-dependent contraction of the IMA obtained from stable as well as unstable patients. It is concluded that unstable angina pectoris is associated with an increased ET-1 turnover. This increased turnover may participate in the local regulation of coronary vascular tone with subsequent influence of the condition of the patients. The present investigation also implies that ET(A)-blockade may be useful as an additional pharmacological principal in the treatment of unstable angina pectoris prior to revascularization, as well as to prevent post-operative arterial graft spasm.

Plasma thioredoxin levels in patients with unstable angina

Advances in Interventional Cardiology