Incidence and evaluation of predisposition to cardiovascular toxicity in chronic myeloid leukemia patients treated with bosutinib in the real-life practice.

There is little information about cardiovascular adverse event (CV-AE) incidence in chronic myeloid leukemia (CML) patients treated with bosutinib in the real-life practice. We identified 54 consecutive CML patients treated with bosutinib, stratified according to the Systematic Coronary Risk Evaluation (SCORE) assessment, based on sex, age, smoking habits, systolic blood pressure, and total cholesterol levels. The 40-month cumulative incidence of CV-AEs was 25.2 ± 8.1%. Patients with the SCORE of high-very high showed a significantly higher incidence of CV-AEs (55 ± 12.9% vs 9 ± 9.5%; p = 0.002). Overall, 9 CV-AEs were reported, with 2 deaths attributed to CV-AE. In conclusion, the SCORE assessment before starting treatment is helpful in identifying CV-AE high-risk patients during bosutinib treatment.

Differential incidence and morphology of provoked spasm between intracoronary acetylcholine and ergonovine testing: recommendation of supplementary use.

When cardiologists diagnose patients with coronary spastic angina, Japanese Circulation Society (JCS) guidelines recommend the intracoronary injection of acetylcholine (ACh) and ergonovine (ER) as class I. However, the pharmacological difference between ACh and ER is controversial in the clinic. We performed both ACh and ER tests in the same 528 patients during 26 years. We investigated the provoked spasm configuration, spasm site, and clinical characteristics of provoked spasm between ACh and ER, retrospectively. We defined positive spasm as ≥90% luminal narrowing. Provoked positive spasm was observed in 161 right coronary arteries (RCA) including 83 ACh just positive, 35 ER just positive, and 43 both positive. In contrast, positive spasm was documented in 172 left coronary arteries (LCA) including 94 ACh just positive, 28 ER just positive, and 50 both positive. ACh provoked spasm more distally and diffusely, while ER induced spasm more proximally and totally or focally in the RCA. In the LCA, ACh provoked spasm more proximally, whereas ER induced spasm more distally. ER testing after the negative ACh tests of RCA and LCA documented new positive spasms in 10.3% (35/340) and 7.4% (28/376), respectively. Coronary artery trees may each have a sensitive receptor on each segment. We recommend the supplementary use of ACh and ER to document coronary artery spasm in the cardiac catheterization laboratory.

Patients with acute myocardial infarction and non-obstructive coronary arteries: safety and prognostic relevance of invasive coronary provocative tests.

Aims: Functional alterations of epicardial coronary arteries or coronary microcirculation represent a frequent cause of myocardial infarction and non-obstructive coronary arteries (MINOCA). We aimed at assessing the prognostic value of intracoronary provocative tests in patients presenting with MINOCA and in which other causes of MINOCA have been excluded. Methods and results: We prospectively evaluated patients with a diagnosis of MINOCA, excluding patients with aetiologies other than suspected coronary vasomotor abnormalities. Immediately after coronary angiography, an invasive provocative test using acetylcholine or ergonovine was performed. The incidence of death from any cause, cardiac death, and recurrence of acute coronary syndrome (ACS) was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). We enrolled 80 consecutive patients [mean age 63.0 ± 10.7 years, 40 (50%) male]. Provocative test was positive in 37 (46.2%) patients without any complication. Among patients with a positive test, epicardial spasm was detected in 24 (64.9%) patients and microvascular spasm in 13 (35.1%) patients. After a median follow-up of 36.0 (range 12.0-60.0) months, patients with a positive test had a significantly higher occurrence of death from any cause [12 (32.4%) vs. 2 (4.7%); P = 0.002], cardiac death [7 (18.9%) vs. 0 (0.0%); P = 0.005], and readmission for ACS [10 (27.0%) vs. 3 (7.0%); P = 0.015] as well as a worse angina status as assessed by SAQ [Seattle score: 88.0 (33.0-100.0) vs. 100.0 (44.0-100.0); P = 0.001] when compared with patients with a negative test. Conclusions: We demonstrate that in patients presenting with MINOCA and suspected coronary vasomotor abnormalities, a positive provocative test for spasm is safe and identifies a high-risk subset of patients.

Fluconazole-Induced Type 1 Kounis Syndrome.

The administration of fluconazole is commonly used in both inpatient and outpatient settings for the management of candidiasis infection. Although it is associated with a relatively safe side effect profile, some patients experience adverse effects associated with increased morbidity. We describe 1 such patient, a 42-year-old woman with a history of severe eczema who developed fluconazole-induced type 1 Kounis syndrome. Review of literature indicates that this as the first case reported of fluconazole-induced type 1 Kounis syndrome.

Comparison of anti-anginal effect of cilnidipine with those of nicardipine and nifedipine in the vasopressin-induced angina model of rats.

We assessed the anti-anginal effects of cilnidipine in comparison with those of nicardipine and nifedipine (1 and 10 µg/kg, n = 6 for each drug) or vehicle (n = 6) by using the vasopressin-induced angina model of rats. The administration of vasopressin (0.5 IU/kg, i.v.) to the rats depressed the S-wave level of the electrocardiogram reflecting the presence of subendocardial ischemia, whereas it significantly increased the mean blood pressure, resulting in the decrease of the heart rate and the prolongation of the PR interval possibly through a reflex-mediated increase in vagal tone. Cilnidipine suppressed the vasopressin-induced depression of the S-wave level in a dose-related manner, which was not observed by nicardipine or nifedipine. In addition, the low dose of cilnidipine hardly affected the vasopressin-induced pressor response, but it attenuated the negative dromotropic effect, suggesting N-type Ca2+ channel inhibition by cilnidipine might have suppressed the parasympathetic nerve activity in vivo like those reported in the sympathetic nerve. Thus, cilnidipine may become a useful strategy for inhibiting coronary vasospasm-induced anginal attack.

Effects of Long-Term Exposure to Ambient Formaldehyde on Hypertension and Angina Pectoris Symptoms: Evidence From the WHO SAGE Cohort Study.

BACKGROUND: We aimed to investigate the associations of long-term exposure to ambient formaldehyde with hypertension and angina pectoris symptoms in Chinese adults. METHODS AND RESULTS: Participants' information was obtained from the WHO SAGE (World Health Organization Study on Global Aging and Adult Health) study. The Cox proportional hazards regression model was applied to estimate the associations of formaldehyde with hypertension and angina pectoris symptoms. Mediating effect analysis was used to investigate the mediating effect of hypertension between formaldehyde exposure and angina pectoris symptoms. Long-term exposure to formaldehyde was positively associated with the risk of angina pectoris symptoms (hazard ratio [HR], 1.66 [95% CI, 1.29-2.13], per interquartile range [IQR], 3.33, 1015 molecules/cm2) and hypertension (HR, 1.17 [95% CI, 1.02-1.34], per IQR, 3.34, 1015 molecules/cm2). The associations between formaldehyde and angina pectoris symptoms were greater in participants aged ≥65 years (HR, 1.90 [95% CI, 1.29-2.80]) and in rural areas (HR, 2.71 [95% CI, 1.54-4.77]), whereas the associations of formaldehyde with hypertension were stronger in men (HR, 1.27 [95% CI, 1.02-1.58]), rural areas (HR, 1.22 [95% CI, 0.94-1.59]), and in ever smokers (HR, 1.33 [95% CI, 1.02-1.72]). The mediation effect analysis indicated that 18.44% (95% CI, 2.17-37.65) of the association between formaldehyde exposure and angina pectoris symptoms was mediated by hypertension. CONCLUSIONS: Long-term exposure to ambient formaldehyde was positively associated with hypertension and angina pectoris symptoms. The effects of formaldehyde may be modified by age, sex, urbanicity, and smoking status. Hypertension might play a mediating effect in formaldehyde-induced angina pectoris symptoms.

The pharmacological differences in antianginal effects of long-lasting calcium channel blockers: azelnidipine and amlodipine.

We examined antianginal effects of azelnidipine and amlodipine in an arginine vasopressin-induced rat anginal model. Oral administration of azelnidipine or amlodipine produced long lasting inhibition of arginine vasopressin-induced ST-segment depression in electrocardiogram. The degrees of inhibition with azelnidipine at doses of 1 and 3 mg/kg were comparable to those with amlodipine at 3 and 10 mg/kg. Both drugs lowered mean blood pressure in a dose-related manner, whereas only azelnidipine decreased heart rate. Azelnidipine at 3 mg/kg and amlodipine at 10 mg/kg produced a similar decrease in the rate pressure product, an index for cardiac oxygen consumption. Their inhibitory effects on calcium-induced vascular contraction were compared in isolated porcine coronary arteries. Both drugs produced a slow-developing inhibition of calcium-induced contraction. Although their inhibitory effects were similar, the way the both drugs inhibited calcium-induced contraction differed with each other. After removing the drug from bathing solution, the inhibitory effects of azelnidipine were not blunted but were sustained for a long time, which indicates that azelnidipine has high vascular affinity. On the other hand, those of amlodipine were rapidly blunted. These results suggest that the mechanisms underlying antianginal effects of azelnidipine differ from those of amlodipine. The antianginal effect with azelnidipine may be accounted for by its high affinity to the coronary blood vessels and the heart rate slowing effect, both of which are not shared with amlodipine.

Association of air pollution and use of glyceryl trinitrate against angina pectoris: a population-based case-crossover study.

BACKGROUND: Ambient air pollution has been associated with increased cardiovascular morbidity and mortality. In Reykjavik, Iceland, air pollutant concentrations exceed official health limits several times every year. The aim was to study the association of concentrations of NO2, O3, PM10, and H2S in the Reykjavik capital area with the dispensing of anti-angina pectoris medication, glyceryl trinitrate to the inhabitants. METHODS: Data on daily dispensing of glyceryl trinitrate, were retrieved from the Icelandic Medicines Registry. Data on hourly concentrations of NO2, O3, PM10, and H2S were obtained from the Environment Agency of Iceland. A case-crossover design was used, based on the dispensing of glyceryl trinitrate to 5,246 individuals (≥18 years) between 2005 and 2009. RESULTS: For every 10 µg/m3 increase of NO2 and O3 3-day mean concentrations, the odds ratio (OR) for daily dispensing of glyceryl trinitrates was 1.136 (95% confidence intervals (CI) 1.069-1.207) and 1.094 (95% CI 1.029-1.163) at lag 0, and OR was 1.096 (95% CI 1.029-1.168) and 1.094 (95% CI 1.028-1.166) at lag 1, respectively. CONCLUSIONS: These findings suggest that NO2 and O3 ambient air concentrations may adversely affect cardiovascular health, as measured by the dispensing of glyceryl trinitrates for angina pectoris. Further, the findings suggest that data on the dispensing of medication may be a valuable health indicator when studying the effect of air pollution on cardiovascular morbidity.

Comparative cardiac toxicity in two treatment schedules of 5-FU/LV for colorectal carcinoma.

The purpose of the study is evaluation and assessment of parameters of cardiac toxicity in patients subjected to 5-FU based chemotherapy. Cardiac morbidity is a reported outcome in different 5FU/LV regimens; however none of them are definite or proximate. The bimonthly regimen of high dose leucovorin is reported to be less toxic and more effective as compared to the monthly regimen of low dose leucovorin. We report the detailed assessment of few cardiac parameter of toxicity in patients of advanced colorectal carcinoma subjected to two Schedules of high and low dose Folinic Acid, 5-Fluorouracil, bolus and continuous infusion. The correlation of elevated cardiac biomarkers, angina and hypertension is comparatively assessed in patients with normal general status, hyperglycemia and known cardiac disorders subjected to two different 5FU based chemotherapeutic regimen.

A systematic review and meta-analysis of air pollution and angina pectoris attacks: identification of hazardous pollutant, short-term effect, and vulnerable population.

We conducted a systematic review and meta-analysis of global epidemiological studies of air pollution and angina pectoris, aiming to explore the deleterious air pollutant(s) and vulnerable sub-populations. PubMed and Web of Science databases were searched for eligible articles published between database inception and October 2021. Meta-analysis weighted by inverse-variance was utilized to pool effect estimates based on the type of air pollutant, including particulate matters (PM2.5 and PM10: particulate matter with an aerodynamic diameter ≤ 2.5 µm and ≤ 10 µm), gaseous pollutants (NO2: nitrogen dioxide; CO: carbon monoxide; SO2: sulfur dioxide, and O3: ozone). Study-specific effect estimates were standardized and calculated with percentage change of angina pectoris for each 10 µg/m3 increase in air pollutant concentration. Twelve studies involving 663,276 angina events from Asia, America, Oceania, and Europe were finally included. Meta-analysis showed that each 10 µg/m3 increase in PM2.5 and PM10 concentration was associated with an increase of 0.66% (95%CI: 0.58%, 0.73%; p < 0.001) and 0.57% (95%CI: 0.20%, 0.94%; p = 0.003) in the risk of angina pectoris on the second day of exposure. Adverse effects were also observed for NO2 (0.67%, 95%CI: 0.33%, 1.02%; p < v0.001) on the second day, CO (0.010%, 95%CI: 0.006%, 0.014%; p < 0.001). The elderly and patients with coronary artery disease (CAD) appeared to be at higher risk of angina pectoris. Our findings suggest that short-term exposure to PM2.5, PM10, NO2, and CO was associated with an increased risk of angina pectoris, which may have implications for cardiologists and patients to prevent negative cardiovascular outcomes.

Exogenous testosterone, cardiovascular events, and cardiovascular risk factors in elderly men: a review of trial data.

INTRODUCTION: Increasing interest in the use of supplemental testosterone has led to a heightened focus on the safety of testosterone in elderly males, with a particular emphasis on cardiovascular risk. AIMS: To evaluate, based on available clinical trial data, whether exogenous testosterone administration in middle-aged to elderly men increases cardiovascular risk, and to assess whether these effects differ in hypogonadal vs. eugonadal subjects. METHODS: MEDLINE search from 2004 to present of all meta-analyses and randomized, controlled clinical trials of testosterone administration in male subjects ≥ 45 years old that included measurements of cardiovascular outcomes or known cardiovascular risk factors before and after treatment with testosterone. MAIN OUTCOME MEASURES: The effects of testosterone treatment on cardiovascular events and cardiovascular risk factors were assessed. RESULTS: In clinical trials where testosterone has been used in patients with preexisting cardiovascular conditions, the effect on disease symptoms has typically been either neutral or beneficial. Based on clinical trial data, testosterone treatment has minimal effect on cardiovascular risk factors with the exception of an increase in hematocrit, which is consistently seen with testosterone treatment, and a decrease in high-density lipoprotein cholesterol, which is an inconsistent response. Responses of hypogonadal and eugonadal men to testosterone treatment in terms of cardiovascular risk are generally similar. Testosterone treatment has not been reported to increase the incidence of cardiovascular events with the possible exception of one trial in frail elderly men. CONCLUSIONS: Available clinical trial data indicate that the use of testosterone in middle-aged to elderly men does not increase cardiovascular risk nor does it unfavorably modify cardiovascular risk profile. Prospective data from large, well-designed, long-term trials of testosterone treatment are lacking and will be required to verify the cardiovascular efficacy/safety of chronic treatment.

[Ergotamine poisoning: a case study]. / Zatrucie ergotamina: opis przypadku.

Ergotamine is a well known pharmacological remedy applied in neurology (treatment of vascular headache) and in obstetrics (abortive remedy, uterus atony). But today it is rarely used, because of new safer anti-migraine medicine (triptanes) which cause fewer side effects. According to obstetrical indications ergotamine is applied only in hospital treatment. For that reason, cases of intoxication by this class of drugs are rarely observed. Ergotamine causes constriction of the blood vessels through the blockade of alpha-receptors and stimulation of the serotonin-receptors on the walls of blood vessels both in the central nervous system and in peripheral circulation. Intoxication/overdose symptoms may appear on application of therapeutic dose by sensitive patients, mostly by patients with migraine headache using ergotamine preparation for relief of migraine attacks. In the Regional Centre of Clinical Toxicology, a 21-year-old patient was hospitalized. She took about 20 tablets of Cafergot (complex preparation containing 1mg ergotamine tartare and 100mg caffeine). During her stay on the ward, typical symptoms of severe poisoning were observed: nausea, severe vomiting, dizziness, decreased blood pressure without perceptible pulse, narrowing of the blood vessels in the extremities of the body (peripheral vasoconstriction) - paresthesia, digital cyanosis, refrigeration of legs, angina. Due to taking once of a great dose of the drug by the patient, violent process of intoxication, possibility of dangerous complication and also the unavailability of specific antidotes and lack of efficient methods of extracorporeal elimination of the drug, the patient was intensively controlled and symptomatic treatments according to the law of intensive therapy was applied.

Dihydroergotamine-induced vasospastic angina in a patient taking a calcium channel blocker.

OBJECTIVE: To report a probable case of vasospastic angina after administration of dihydroergotamine mesylate in a patient without coronary artery disease. CASE SUMMARY: A 49-year-old woman with relapsing/remitting multiple sclerosis was admitted for severe headache and pain crisis. She received a single dose of intravenous dihydroergotamine and, within 30 minutes, experienced chest pain, nausea, and vomiting. No changes on electrocardiogram were noted, but cardiac enzyme levels were elevated. Brief episodes of chest pain persisted for several days and resolved spontaneously before the woman's discharge. She had several cardiac risk factors, including cigarette smoking, hypertension, and a family history of coronary artery disease, but cardiac catheterization on hospital day 5 revealed no underlying coronary artery disease. DISCUSSION: Although cardiovascular adverse reactions have been reported with ergotamine tartrate, dihydroergotamine has rarely been linked with such reactions, including coronary vasospasm and myocardial infarction. Prescribing information for dihydroergotamine cautions against its use in patients with coronary artery disease or risk factors for underlying coronary artery disease without a cardiac workup before initiation of therapy. This patient had several cardiac risk factors, but cardiac catheterization revealed no underlying coronary artery disease. Concomitant verapamil therapy for hypertension did not prevent the vasospastic effects of dihydroergotamine. The Naranjo probability scale revealed a probable adverse reaction of vasospastic angina associated with dihydroergotamine. CONCLUSIONS: Health-care professionals should be aware of the possibility for vasospastic angina in patients receiving dihydroergotamine who have no underlying coronary artery disease. Prescribing information should be closely followed.

Cardiovascular disease risk associated with asthma and respiratory morbidity might be mediated by short-acting beta2-agonists.

BACKGROUND: Studies examining the asthma-related risks of cardiovascular disease (CVD) events have generally used selected samples or did not control for the effects of beta(2)-agonist use, itself associated with CVD events. OBJECTIVES: We assessed the relationship between incident CVD/stroke and asthma and the effect of atopy while controlling for beta(2)-agonist use in a representative adult population cohort free of CVD at baseline. METHODS: The North West Adelaide Health Study (stage 1, n = 3812; stage 2, n = 3113) assessed spirometry, anthropometry, atopy, blood pressure, and lipid levels. Questionnaires assessed doctor-diagnosed asthma and CVD (myocardial infarction and angina)/stroke, smoking status, and demographics. Asthma was defined by self-report or FEV(1) reversibility. Current short- and long-acting beta(2)-agonist use was identified at follow-up. RESULTS: Results are expressed as odds ratios (ORs) and 95% CIs. By using multivariable logistic regression, after adjustment for risk factors, in female subjects incident CVD/stroke events were associated with asthma (OR, 3.24; 95% CI, 1.55-6.78), with no effect modification by atopy (P for interaction = .61), and with as-required short-acting beta(2)-agonist use (OR, 2.66; 95% CI, 1.06-6.61). In male subjects events were associated with daily cough/sputum (OR, 1.92; 95% CI, 1.05-3.50) and FEV(1) of less than 80% of predicted value but an FEV(1)/forced vital capacity ratio of greater than 0.70 (OR, 2.15; 95% CI, 0.91-5.09; P = .08). Although few CVD/stroke events occurred in male subjects with asthma, a significant interaction with atopic status was found (P = .05). CONCLUSIONS: Studies are required to elucidate how asthma exposes older women to excess macrovascular risk and prospectively determine the short-acting beta(2)-agonist-related risk in persons without existing CVD. CVD risk in relation to atopic status of asthma also requires further investigation.

[A case of recurrent colon cancer with angina pectoris and interstitial pneumonia during cetuximab therapy with death by carcinomatous lymphangiosis].

The case was a man in his 60s with no past history of heart and lung. Chest tightness was felt during the first course of cetuximab therapy for recurrent colon cancer. He was diagnosed as having vasospastic angina, and administration of vasodilatation agents was done. After the therapy, no chest pain attack was seen. Chemotherapy was continued. After 3 courses, fever elevation, chest tightness and dyspnea were seen. Chest X-ray and CT revealed diffuse interstitial pneumonia in bilateral lung. Although steroid pulse therapy and intensive therapy with mandatory ventilation were performed, he died of respiratory failure. Pathological findings of autopsy revealed remarkable metastasis of cancer cells to the bilateral lungs accompanied chiefly with carcinomatous lymphangiosis. Furthermore, acute and subacute interstitial pneumonia with diffuse alveolar damage were seen in the background of the lungs. Cardiopulmonary disorder as well as skin disorder should be considered as possible adverse events of cetuximab therapy.

Greater Odds for Angina in Uranium Miners Than Nonuranium Miners in New Mexico.

OBJECTIVE: The aim of this study was to test the hypothesis that uranium miners in New Mexico (NM) have a greater prevalence of cardiovascular disease than miners who extracted the nonuranium ore. METHODS: NM-based current and former uranium miners were compared with nonuranium miners by using cross-sectional standardized questionnaire data from the Mining Dust in the United States (MiDUS) study from 1989 to 2016. RESULTS: Of the 7215 eligible miners, most were men (96.3%). Uranium miners (n = 3151, 43.7%) were older and diabetic, but less likely to currently smoke or use snuff (P ≤ 0.001 for all). After adjustment for covariates, uranium miners were more likely to report angina (odds ratio 1.51, 95% confidence interval 1.23 to 1.85) than nonuranium miners. CONCLUSION: Our data suggest that along with screening for pulmonary diseases, uranium industry workers should be screened for cardiovascular diseases.

Mentha longifolia alleviates experimentally induced angina via decreasing cardiac load.

Angina occurs due to imbalance between heart oxygen demand and supply and is associated with serious morbidity and mortality. Here, the possible antianginal effect of Mentha longifolia extract was studied in experimental model of angina. Aerial parts of M. longifolia were extracted, standardized, and given to rats three days before angina. Heart hemodynamics and conductivity were recorded by microtip catheter and surface electrodes. M. longifolia extract significantly alleviated the sustained decline in cardiac contractility after vasopressin exposure. However, M. longifolia did not affect the impaired cardiac dilation after vasopressin. Heart rate was significantly decreased after vasopressin exposure in rats treated with M. longifolia compared with untreated animals. In addition, M. longifolia produced more increase in systolic and diastolic durations after vasopressin exposure compared with untreated animals. Moreover, the plant extract alleviated the ST height changes during vasopressin injection. M. longifolia extract alleviates impaired cardiac function associated with angina through decreasing heart work. PRACTICAL APPLICATIONS: The present study is the first to study the effect of M. longifolia in an experimental model of angina. M. longifolia alleviated the impaired cardiac contractility associated with angina exposure. The antianginal effect of M. longifolia could be through reducing cardiac load. This can be concluded from the decrease in heart rate and the systolic and diastolic cycles elongation after exposure to vasopressin in animals pretreated with M. longifolia. This helps in reducing the associated cardiac ischemia upon exposure to vasopressin as indicated by ST change. This could provide new directions in the management of the serious angina disease.

Intramyocardial transplantation of autologous CD34+ stem cells for intractable angina: a phase I/IIa double-blind, randomized controlled trial.

BACKGROUND: A growing population of patients with coronary artery disease experiences angina that is not amenable to revascularization and is refractory to medical therapy. Preclinical studies have indicated that human CD34+ stem cells induce neovascularization in ischemic myocardium, which enhances perfusion and function. METHODS AND RESULTS: Twenty-four patients (19 men and 5 women aged 48 to 84 years) with Canadian Cardiovascular Society class 3 or 4 angina who were undergoing optimal medical treatment and who were not candidates for mechanical revascularization were enrolled in a double-blind, randomized (3:1), placebo-controlled dose-escalating study. Patients received granulocyte colony-stimulating factor 5 microg x kg(-1) x d(-1) for 5 days with leukapheresis on the fifth day. Selection of CD34+ cells was performed with a Food and Drug Administration-approved device. Electromechanical mapping was performed to identify ischemic but viable regions of myocardium for injection of cells (versus saline). The total dose of cells was distributed in 10 intramyocardial, transendocardial injections. Patients were required to have an implantable cardioverter-defibrillator or to temporarily wear a LifeVest wearable defibrillator. No incidence was observed of myocardial infarction induced by mobilization or intramyocardial injection. The intramyocardial injection of cells or saline did not result in cardiac enzyme elevation, perforation, or pericardial effusion. No incidence of ventricular tachycardia or ventricular fibrillation occurred during the administration of granulocyte colony-stimulating factor or intramyocardial injections. One patient with a history of sudden cardiac death/ventricular tachycardia/ventricular fibrillation had catheter-induced ventricular tachycardia during mapping that required cardioversion. Serious adverse events were evenly distributed. Efficacy parameters including angina frequency, nitroglycerine usage, exercise time, and Canadian Cardiovascular Society class showed trends that favored CD34+ cell-treated patients versus control subjects given placebo. CONCLUSIONS: A randomized trial of intramyocardial injection of autologous CD34+ cells in patients with intractable angina was completed that provides evidence for feasibility, safety, and bioactivity. A larger phase IIb study is currently under way to further evaluate this therapy.

Heparin-induced thrombocytopenia (HIT) causing pulmonary emboli during coronary intervention.

Thrombotic complications of heparin-induced thrombocytopenia (HIT) can be devastating if not recognized and treated promptly. We describe an unusual case of rapid-onset HIT resulting in massive-bilateral pulmonary emboli in a 70 year-old man who developed chest pain during elective percutaneous coronary intervention (PCI). The diagnosis was made the following day after persistent chest pain and laboratory work demonstrating a new thrombocytopenia, a mildly elevated troponin, and positive DIC panel led to confirmatory imaging tests. HIT-related thrombosis should be considered in the differential diagnosis of chest pain in patients undergoing PCI.