Ventricular septal rupture with "normal" coronary arteries

A 73-year-old woman was admitted to St. Margaret's Hospital with a history of an acute anteroseptal infarction, a loud cardiac murmur, and low cardiac output. Cardiac catheterization revealed a large, high ventricular septal defect and normal coronary arteries. Despite successful closure of the ventricular septal rupture, death occurred in the operating room due to severe right ventricular dysfunction. Although this patient had normal major coronary arteries, a ventricular septal rupture developed, which was probably caused by spasm or isolated atherosclerotic disease of a large septal perforator.     

Chest pain and electrocardiographic ST-segment elevation occurring in the recovery phase after exercise in a patient with normal coronary arteries

Exercise-induced ST-segment elevation usually occurs in patients with coronary artery disease. We report a case in which ST-segment elevation occurred during the recovery phase of exercise in a patient with normal coronary arteries.     

Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries

Forty-one patients with chest pain and angiographically normal coronary arteries were studied for platelet abnormalities. Patients with conditions known or suspected to be associated with chest pain or platelet dysfunction were excluded. After coronary angiography and 2-week withdrawal from all medications, platelet aggregometry was performed using peripheral venous plasma samples and 3 concentrations of adenosine diphosphate, 2.34, 1.17 and 0.58 μM, and epinephrine, 11, 1.1 and 0.55 μM, as stimuli. Platelet morphology in response to surface contact (adhesion) was evaluated by transmission electron microscopy to determine the percentage of platelets in the round/abortive (inactive), dendritic (intermediate) and spread (activated) forms. Plasma specimens obtained from healthy volunteers of similar age and sex were analyzed in parallel and served as control subjects. Compared with control subjects, patients had increased aggregation at all concentrations of both adenosine diphosphate and epinephrine (p < 0.001). Patients also had fewer platelets in the dendritic form and more in the round/abortive and spread forms. Thus, patients with chest pain and normal coronary arteries have platelet hyperaggregability in vitro, although the clinical relevance of this finding is unclear.     

Abnormal cardiac sensitivity in patients with chest pain and normal coronary arteries

The causes of chest pain in patients found to have angiographically normal coronary arteries during cardiac catheterization remain controversial. Cardiac sensitivity to catheter manipulation, pacing at various stimulus intensities and intracoronary injection of contrast medium was examined in several groups of patients who underwent cardiac catheterization. Right heart (especially right ventricular) catheter manipulation and pacing and intracoronary contrast medium provoked chest pain typical of that previously experienced in 29 (81%) of 36 patients with chest pain and angiographically normal coronary arteries and 15 (46%) of 33 symptomatic patients with hypertrophic cardiomyopathy. In contrast, only 2 (6%) of 33 symptomatic patients with coronary artery disease experienced their typical chest pain with these sensitivity tests (p less than 0.001). None of 10 patients with valvular heart disease but without a chest pain syndrome experienced any sensation with these tests. Cutaneous pain threshold testing demonstrated that patients with chest pain and normal coronary arteries had a higher pain threshold to thermal stimulation compared with patients who had coronary artery disease or hypertrophic cardiomyopathy. No relation existed between cardiac sensitivity and cutaneous sensitivity testing. Thus, patients who have chest pain despite angiographically normal coronary arteries may have abnormal cardiac sensitivity to a variety of stimuli. This increased sensitivity may be of causal importance to their chest pain syndrome or may contribute to their perception of ischemia-induced pain. The same phenomenon was also commonly seen in symptomatic patients with hypertrophic cardiomyopathy. Whether this phenomenon represents abnormal activation of pain receptors within the heart or abnormal processing of visceral afferent neural impulses in the peripheral or central nervous system is unknown.     

Endothelial dysfunction in patients with chest pain and normal coronary arteries.

BACKGROUND. A subgroup of patients with chest pain and angiographically normal epicardial coronary arteries have reduced dilator response to metabolic or pharmacological stimuli, but the mechanisms responsible for this reduced dilator response are unknown. In this study, we have investigated whether microvascular endothelial dysfunction is a cause of the observed reduced vasodilator reserve. METHODS AND RESULTS. The functional response of the microvasculature was studied with rapid atrial pacing at 150 beats per minute. Fifty-one patients, 20 hypertensive and 31 normotensive, with chest pain and normal epicardial coronary arteries (< 10% stenosis) were studied. Endothelial function was tested with incremental infusions of acetylcholine to achieve estimated intracoronary concentrations ranging from 10(-7) M to 10(-5) M. Endothelium-independent smooth muscle vasomotion was measured using intracoronary sodium nitroprusside. Endothelial dysfunction of epicardial coronary arteries, demonstrated as severe (> 50%) constriction with < 10(-5) M acetylcholine concentration, was evident in five patients (10%). In the remaining 46 patients, coronary blood flow increased with acetylcholine (mean, 78 +/- 43%) and atrial pacing (mean, 51 +/- 37%), and coronary vascular resistance decreased by 35 +/- 16% and 29 +/- 14%, respectively, but the responses were heterogeneous. There was a correlation between the coronary resistance change with acetylcholine and the change with atrial pacing: r = 0.68, p < 0.001 in these 46 patients. Thus, patients with depressed dilation with atrial pacing had reduced endothelium-dependent dilation with acetylcholine, and vice versa. However, the microvascular dilation caused by sodium nitroprusside was not significantly different between patients with and those without reduced dilation with atrial pacing, indicating that the vasodilator defect was not caused by smooth muscle dysfunction. There were no differences in the vasodilator responses with atrial pacing, acetylcholine, or nitroprusside between normotensive and hypertensive patients. Multivariate regression analysis was performed to determine whether age, sex, serum cholesterol level, hypertension, presence of mild epicardial vessel atherosclerosis, resting left ventricular function, change in left ventricular ejection fraction with exercise, vasodilation with acetylcholine, and vasodilation with sodium nitroprusside were independently related to the vasodilator response to atrial pacing. Only the change in coronary vascular resistance with acetylcholine was independently correlated with the change in resistance with atrial pacing: R2 = 0.46, p < 0.0001. CONCLUSIONS. Patients with chest pain, normal epicardial coronary arteries, and reduced vasodilation in response to atrial pacing appear to have associated endothelial dysfunction of the coronary microvasculature. Thus, microvascular endothelial dysfunction may contribute to the reduced vasodilator reserve with atrial pacing and anginal chest pain in these patients.     

Panic disorder in patients with chest pain and angiographically normal coronary arteries

Although patients with angiographically normal or near normal coronary arteries are at low risk for cardiac disease, several follow-up studies have shown that many continue to report recurrent chest pain associated with social and work dysfunction. Three diagnostic entities have been proposed to explain the morbidity of this group: microvascular angina, esophageal motility disorders and panic disorder. The purpose of this study was to test the hypothesis that panic disorder is found frequently in patients with chest pain who have normal epicardial vessels. Ninety-four subjects with angiographically normal coronary arteries were interviewed according to a structured psychiatric protocol within 24 hours of their catheterizations. Thirty-two (34%) fit Diagnostic and Statistical Manual of Mental Disorders (third edition, revised) criteria for current panic disorder. Because panic disorder can be effectively treated, physicians should consider this diagnosis in this group of patients. Current research findings suggest that panic disorder, microvascular angina and esophageal disorders may each form the basis for chest pain in approximately 25% of these patients. Miscellaneous problems account for the other 25%.     

Stenting small coronary arteries

Stenting of small coronary arteries was long contra-indicated because of a high rate of subacute occlusion. We report a single-center registry including 190 patients stented with 2.5 mm balloons. Procedural success was 98% and subacute occlusion rate was 2.6%. Clinical follow-up showed a 24.5% repeat intervention rate. These results seemed acceptable, warranting stent implantation in small arteries in the case of acute or threatened closure. New stent designs and coatings may contribute to the improvement of outcomes and to the decrease in subacute occlusion and restenosis rates.     

One-year psychosocial follow-up of patients with chest pain and angiographically normal coronary arteries

As many as 30% of patients with chest pain symptoms who are referred for arteriography are found to have normal coronary arteries. Research has shown that patients with anginal symptoms and normal coronary arteries score higher on neuroticism measurements (anxiety, depression and somatic concerns) at the time of catheterization than patients with anginal symptoms who have coronary artery disease. Research examining the cardiac course of chest pain patients with normal coronary arteries indicates that this is a nonprogressive disorder. Although follow-up studies of these patients report continued chest pain and diminished physical activity, these studies have ignored the psychologic status of the patients. Thus, it is not known whether their higher neuroticism scores at the time of catheterization persist following angiography or whether such elevated indexes of neuroticism are transient phenomena associated with precatheterization anticipatory stress. The present study examined 48 Veterans Administration Medical Center patients: 24 with anginal symptoms and normal coronary arteries and 24 with documented coronary artery disease. The patients completed a structured clinical interview and a set of psychologic inventories on the day before catheterization and 1 year later. The findings established continued high neuroticism scores among patients with anginal symptoms only and supported the findings of other investigators regarding continuing chest pain and restricted physical activity. The knowledge alone of benign coronary artery status resulted in virtually no change in the psychosocial status of these patients. Alternative treatment methods are discussed.     

Coronary flow reserve in patients with chest pain and normal coronary arteries.

BACKGROUND--Many studies have shown that coronary flow reserve is reduced in patients with chest pain and angiographically normal coronary arteries. The methods used to assess coronary blood flow have varied, but in nearly all reports dipyridamole has been used to bring about vasodilatation. This study was designed to assess whether the apparent impairment of coronary flow reserve seen with dipyridamole could be reproduced with either papaverine or adenosine, which induce maximum coronary blood flow by different mechanisms. METHODS--25 patients with chest pain and angiographically normal coronary arteries were studied with an intracoronary Doppler flow probe and quantitative angiography to determine epicardial coronary artery area, coronary blood flow velocity, coronary flow reserve, and coronary vascular resistance index (CVRI, the ratio of resistance after intervention to basal resistance). All patients received papaverine 8 mg. Eight patients with positive exercise tests received intracoronary papaverine (8 and 10 mg), intracoronary adenosine (6, 20, 60 micrograms), and high-dose intravenous dipyridamole (0.84 mg/kg). RESULTS--The velocity ratio (peak after intervention: baseline) (mean (SEM)) after 8 mg papaverine was 3.3 (0.2) (n = 25) and the coronary flow reserve was 4.1 (0.3) (n = 25). There were no differences between patients with a positive (n = 16) or negative (n = 9) exercise test. In eight patients coronary flow reserve was measured after increasing doses of papaverine, adenosine, and dipyridamole. Coronary flow reserve was 4.5 (0.3) with papaverine, 4.8 (0.3) with adenosine, and 3.5 (0.4) with dipyridamole (p = 0.08 v papaverine and adenosine). CVRI was 0.22 (0.01) with papaverine, 0.21 (0.02) with adenosine, and 0.29 (0.03) with dipyridamole (p < 0.05 v papaverine, p = 0.09 v adenosine). CONCLUSIONS--These results indicate that measurement of coronary flow reserve and CVRI in patients with chest pain and normal coronary arteries depends on the pharmacological stimulus. Normal values were obtained with papaverine in all patients, irrespective of the exercise test response. In patients with a positive exercise test significantly lower values were obtained with dipyridamole than with papaverine, or adenosine. The reported impairment of coronary flow reserve in patients with angina and normal coronary arteries may reflect the variability in response to different pharmacological agents. The mechanism underlying this variability is unknown, but may involve an abnormality of adenosine metabolism in the myocardium.     

Chest pain after coronary interventional procedures

Chest pain following successful percutaneous coronary interventions is a common problem. Although the development of chest pain after coronary interventions may be of benign character, it is disturbing to patients, relatives and hospital staff. Such pain may be indicative of acute coronary artery closure, coronary artery spasm or myocardial infarction, but may also simply reflect local coronary artery trauma. The distinction between these causes of chest pain is crucial in selecting optimal care. Management of these patients may involve repeat coronary angiography and additional intervention. Commonly, repeat coronary angiography following percutaneous transluminal coronary angioplasty (PTCA) in patients with chest pain demonstrates widely patent lesion sites suggesting that the pain was due to coronary artery spasm, coronary arterial wall stretching or was of non-cardiac origin. As reported by the National Heart, Lung and Blood Institute PTCA Registry, 4.6% of patients after angioplasty have coronary occlusions, 4.8% suffer a myocardial infarction, and 4.2% have coronary spasm. The frequency of chest pain after new device coronary interventions (atherectomy and stenting) seems to be even higher. However, only the minority of patients with post-procedural chest pain have indeed an ischemic event. Therefore, the vast majority of patients have recurrent chest pain without any signs of ischemia. There is some evidence that non-ischemic chest pain after coronary interventions is more common after stent implantation as compared to PTCA (41% vs. 12%). This may be due to the continuous stretching of the arterial wall by the stent as the elastic recoil occurring after PTCA is minimized. In conclusion, chest pain after coronary interventional procedures may potentially be hazardous when due to myocardial ischemia. However, especially after coronary stent placement, cardiologists must consider "stretch pain" due to the overdilation and stretching of the artery caused by the stent in the differential diagnosis. Clinically, it is, therefore, important to recognize that in addition to ischemia-related chest pain other types of chest pain do exist with cardiac origin.     

小冠状动脉狭窄性病变的介入治疗

目的 :探讨小冠状动脉 （直径 <3 mm）狭窄性病变实施普通球囊、切割球囊或小支架介入治疗的疗效和并发症。方法 :小冠脉狭窄性病变介入治疗 （PCI）患者 13 6（男 87,女 49）例 ,年龄 3 2～ 85（54± 17）岁。根据手术方法分为普通球囊组、切割球囊组和小支架组。残余狭窄率 <3 0 %且无动脉夹层、撕裂等并发症者为手术成功 ,术后 6个月复查冠脉造影。结果 :普通球囊组 3 2例 ,手术成功 2 6例 （81% ） ,出现动脉夹层或扩张不满意改支架术 6例 （2 4% ）。切割球囊组 48例 ,手术成功 43例 （90 % ） ,出现动脉夹层或扩张不满意改支架术 3例 ,出现造影剂血管外漏 2例。支架组 56例 ,手术成功 53例 （95% ） ,出现造影剂血管外漏 2例 ,出现心包填塞抢救成功 1例。3组均未出现血管急性闭塞。术后 6个月 ,切割球囊组、小支架组、普通球囊组冠脉造影狭窄率分别为 2 3 % （11例 ）、16% （9例 ）、3 8% （12例 ）。结论 :小冠脉狭窄性病变实施介入治疗能取得显著效果 ,小支架术优于普通球囊扩张术 ,切割球囊扩张与普通球囊扩张具有近似疗效