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.

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.

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.

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.

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.

Successful desensitization to radiocontrast media in two high-risk cardiac patients.

Hypersensitivity reactions to radiocontrast media (RCM) are common and in severe cases may present a challenge for treating physician in cases when premedication fails or the patient presents with severe comorbidities. We describe two cases in need of radiocontrast media after a severe reaction on previous exposure to iohexol. One presented anaphylactic reaction to RCM despite premedication and another presented with angina. Both cases were treated with a desensitization protocol to iodixanol. In conclusion, desensitization to radiocontrast media may be considered in patients with previously unsuccessful premedication and/or severe acute comorbidities. SIMILAR CASES PUBLISHED: 14.

[Cardiac arrest induced by vasospastic angina pectoris after vaginally administered misoprostol].

A 41-year-old woman developed cardiac arrest after administration of misoprostol in order to induce an abortion. She was successfully resuscitated. Coronary angiography revealed coronary artery spasm which responded to nitroglycerine. Misoprostol is first-line treatment for medically induced abortion. Reports have described cardiovascular adverse events in women with cardiovascular risk factors, and clinicians should be aware of this.

Cannabis: Exercise performance and sport. A systematic review.

OBJECTIVES: To review the evidence relating to the effect of cannabis on exercise performance. DESIGN: A systematic review of published literature METHODS: Tetrahydrocannabinol (THC) is the principal psychoactive component of cannabis. A search was conducted using PUB med, Medline and Embase searching for cannabis, marijuana, cannabinoids and THC, in sport and exercise; the contents of sports medicine journals for the last 10 years; as well as cross references from journals and a personal collection of reprints. Only English language literature was reviewed and only articles that specified the details of a formal exercise program or protocol. Individuals in rehabilitation or health screening programs involving exercise were included as the study may have identified adverse reactions in the marijuana group. Review articles, opinion pieces, policy statements by sporting bodies and regulatory agencies were excluded. RESULTS: Only 15 published studies have investigated the effects of THC in association with exercise protocols. Of these studies, none showed any improvement in aerobic performance. Exercise induced asthma was shown to be inhibited. In terms of detrimental effects, two studies found that marijuana precipitated angina at a lower work-load (100% of subjects) and strength is probably reduced. Some subjects could not complete an exercise protocol because adverse reactions caused by cannabis. An important finding relevant to drug testing was that aerobic exercise was shown to cause only very small rises (<1ng/mL) in THC concentrations. CONCLUSIONS: THC does not enhance aerobic exercise or strength.

Impact of vasomotion type on prognosis of coronary artery spasm induced by acetylcholine provocation test of left coronary artery.

BACKGROUND AND AIMS: The impact of vasomotion types on long-term clinical outcomes in patients with coronary artery spasm (CAS) induced by the acetylcholine provocation test (ACH-test) remains unclear. METHODS: We evaluated 4644 consecutive patients with typical resting chest pain (CP), but no angiographically significant coronary artery lesion (<50% stenosis), who underwent an ACH-test. According to their vasomotor response, patients were categorized into four types: normal vasomotion (no CP, no ischemic electrocardiographic changes, and no vasoconstriction), microvascular spasm (CP with <75% vasoconstriction but with CP relief after nitroglycerin infusion), epicardial spasm (CP with ≥75% vasoconstriction), and ACH-test inconclusive (vasoconstriction and/or electrocardiographic changes, but no CP). We investigated CP recurrence requiring follow-up angiography and major adverse cardiovascular events (MACEs) during 5 years. RESULTS: CP recurred in 7.9% of patients and was more frequent in abnormal vasomotion types (normal vasomotion, microvascular spasm, epicardial spasm, and inconclusive type: 5.4%, 9.8%, 10.9%, and 8.2%, respectively, log-rank p = 0.009). In multivariate analysis adjusted for medication use after the ACH-test, vasomotion subtype was not an independent predictor, whereas male sex, fixed lesion on baseline angiography, and medications including calcium channel blockers (CCBs), nitrates, and statins were independent positive predictors for recurrent CP. Alcohol consumption at the initial interview was a negative predictor. MACEs were observed in 1.6%, and the incidence was similar among subtypes (p = 0.421). CONCLUSIONS: Recurrent CP and long-term outcomes are independent of vasomotion subtypes, but long-term use of CCBs, nitrates, and statins is a significant predictor for recurrent CP.

Coronary Spastic Angina Induced after Oral Desmopressin (DDAVP) Administration.

A 60-year-old man was prescribed oral desmopressin (1-deamino-8-D-arginine vasopressin acetate trihydrate; DDAVP) for nocturnal polyuria. One week after starting to take desmopressin, he frequently felt chest pain while resting. Coronary angiography revealed no organic stenosis; however, an acetylcholine provocation test showed severe coronary spasm with ST elevation. He was diagnosed with coronary spastic angina, and we stopped the oral desmopressin and added diltiazem. While DDAVP should dilate the coronary vessels in healthy subjects, it may provoke coronary vasospasm in patients with endothelial dysfunction. We should be careful to avoid triggering coronary spasm when administering DDAVP to patients that may have potential endothelial dysfunction.

Myocardial infarction induced by oral terazosin in a patient with predisposing structural cardiomyopathy: case report. / Infarto agudo de miocardio asociado al uso de terazosina oral en presencia de cardiopatía estructural predisponente: reporte de caso.

We describe a 71-year-old male patient who developed acute myocardial infarction (AMI) due to a dynamic left ventricular outflow tract obstruction induced by terazosin. After receiving terazosin, the patient had a syncope followed by angina. The electrocardiogram showed Q waves and ST segment elevation in the precordial and inferior leads. Coronary angiography evidenced a chronically occluded left anterior descending artery. Doppler-echocardiography revealed apical akinesia, hyperdynamic basal segments, systolic anterior motion of the mitral valve (SAM) and dynamic left ventricular outflow tract obstruction. Therapy with intravenous fluids and atenolol resulted in marked clinical improvement. Acute myocardial infarction resulted from low coronary perfusion pressure in a patient with a chronically diminished coronary reserve.

Describimos el caso de un hombre de 71 años de edad, que presentó un infarto agudo de miocardio debido a la obstrucción dinámica del tracto de salida del ventrículo izquierdo inducida por la terazosina. Luego de recibir dicha medicación el paciente presentó un síncope y posteriormente angina de pecho. El electrocardiograma evidenció ondas Q y sobreelevación del segmento ST en las derivaciones precordiales e inferiores. La angiografía coronaria evidenció una oclusión crónica de la arteria descendente anterior y el ecocardiograma Doppler reveló aquinesia apical, segmentos basales hiperdinámicos, movimiento anterior sistólico de la válvula mitraI y obstrucción dinámica del tracto de salida del ventrículo izquierdo. La administración intravenosa de suero fisiológico y atenolol determinó una clara mejoría clínica. Un infarto agudo de miocardio hemodinámico fue el resultado de la caída de la presión de perfusión coronaria en un paciente con disminución crónica de la reserva coronaria.

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.

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.

[Analysis of cardiovascular diseases after the upload phase with intravitreal ranibizumab and bevacizumab in patients with exudative age-related macular degeneration]. / Analyse kardiovaskulärer Erkrankungen nach der Upload-Phase mit intravitrealem Ranibizumab oder Bevacizumab bei Patienten mit exsudativer altersbedingter Makuladegeneration.

BACKGROUND: The intravitreal administration of vascular endothelial growth factor (VEGF) inhibitors is the gold standard in the treatment of exudative age-related macular degeneration (AMD) but the possible risks of systemic, particularly cardiovascular side effects are still discussed. PATIENTS AND METHODS: We prospectively followed 111 patients at the University Hospital in Göttingen with exudative AMD and intravitreal ocular treatment with bevacizumab and ranibizumab during the upload phase of 3 months using a questionnaire for documentation of possible cardiovascular events. RESULTS: In 5 out of 111 patients angina pectoris was observed and in 6 patients the antihypertensive medication had to be increased. No differences were found between bevacizumab and ranibizumab. A patient with pre-existing cardiovascular diseases suffered a stroke in the upload phase but no thromboembolic events were observed in the other patients. CONCLUSION: In this small but prospective clinical study no increased risk for cardiovascular events during the upload phase of the VEGF inhibitors ranibizumab and bevacizumab could be detected when taking the age and pre-existing cardiovascular diseases into consideration.

Pentoxifylline alleviates cardiac ischemia and dysfunction following experimental angina in insulin resistance.

We have previously shown that pentoxifylline (PTX) protects from vascular complications associated with insulin resistance (IR). Here, we investigated the protective effect of PTX against cardiac ischemia and dysfunction following experimental angina in IR. IR, along with its accompanying cardiac dysfunction, was induced in rats by a high-fructose (10% in drinking water) high-fat diet for 12 weeks. PTX was administered daily (30 mg⋅kg(-1)) during the last 4 weeks of the study. Experimental angina was induced by isoproterenol (10 µg⋅kg(-1)) administered by intravenous injection. Both before (baseline) and after the experimental angina, cardiac contractility was assessed by continuous recording in anesthetized rats via a microtip catheter inserted in the left ventricle, and cardiac conductivity was determined by a surface electrocardiograph. Serum glucose, insulin, tumor necrosis factor-α (TNFα), and adiponectin levels and lipid profile were also determined. Feeding the rats a high-fructose high-fat diet produced IR, as evidenced by significant hyperinsulinemia and hyperglycemia, and PTX administration did not affect this IR. When subjected to experimental angina, IR hearts were less resistant to the ischemia following induction of angina (reflected by the large ST height depression) compared with controls, and PTX completely prevented the excessive ST height depression in IR animals. In addition, left ventricular pressure development was largely attenuated during and after induction of angina in IR animals compared with controls. PTX administration prevented the excessive attenuation in ventricular pressure development in IR animals. IR was associated with elevated levels of the inflammatory cytokine TNFα, whereas PTX treatment elevated the serum level of the anti-inflammatory cytokine adiponectin. PTX alleviates cardiac ischemia and dysfunction following experimental angina in IR directly through inhibition of the low-grade inflammation that accompanies IR.