Reversible Cardiac Dysfunction Research Articles

Evaluation of cardiac function using transthoracic echocardiography in patients with myocardial injury secondary to methomyl poisoning.

Generally, the mortality rate for cases of carbamate poisoning is low, but fatalities secondary to methomyl poisoning have been reported including a case report of cardiac toxicity following short-term exposure to methomyl. There have been no reports, however, regarding patterns of cardiac toxicity after exposure to methomyl. Therefore, we investigated the prevalence and patterns of myocardial injury using a biochemical marker, troponin I (TnI), and evaluated cardiac function using transthoracic echocardiography (TTE). We conducted a retrospective review of 14 consecutive methomyl poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between January 2009 and December 2013. On ECG analysis, ST depression and T-wave inversion were seen in five patients (35.7%) and one patient (7.1%), respectively. On cardiac biochemical marker analysis, initial TnI was elevated in 11 patients (78.6%). TTE was performed in nine patients among the 11 patients in whom TnI was found to be elevated. Of the nine patients that underwent TTE, three patients (33.3%) showed a reduced ejection fraction (EF), and RWMA was noted in two patients. There were two patients (22.2%) that had both reduced systolic function and RWMA. One patient did not regain normal systolic function on admission. None of the three patients with reduced EF received any specific treatment to support cardiac function. One patient expired due to pneumonia, and one patient was transferred as moribund. We followed up on 12 patients who survived to discharge for 6-44 months. One patient (8.3%) was died to follow-up, and 11 patients survived without any further complications. Methomyl exposure can cause direct myocardial injury and reversible cardiac dysfunction. Monitoring of TnI levels and TTE for evaluation of cardiac function may be useful in the workup of patients suffering from methomyl poisoning.

English

Takotsubo cardiomyopathy is a condition caused by intense emotional or physical stress leading to rapid and severe reversible cardiac dysfunction. A 44 year old labourer presented with three days old bilateral traumatic fracture of femur and severe respiratory distress; he was ventilated for one day. Echocardiography ruled out pulmonary embolism. Patient remained stable for the next three days. On the fifth day, he appeared fearful, presented with sudden chest pain, tachycardia and hypotension. Echocardiography revealed ejection fraction of 34%, global hypokinesia of left ventricle with apical ballooning and no regional wall motion abnormalities. Coronary angiography was done which revealed no vascular abnormalities. Diagnosis of Takotsubo cardiomyopathy was made and vasopressors were started. Psychiatric treatment of physical and emotional stress was done. Patient gradually improved with ongoing treatment and on eighth day his cardiac function reverted back to normal. Takotsubo cardiomyopathy can be efficiently managed by early recognition, proper supportive treatment and meticulous management of physical and emotional stress.

Cushing's Disease is associated with reversible cardiac dysfunction and remodelling assessed by CMR

Background Cardiovascular complications are the main cause of death in chronic hypercorticism. Cushing’s disease (CD) is caused by a benign pituitary gland secreting tumor resulting in endogen hypercorticism. Few ultrasound studies have described cardiac involvement in Cushing’s disease, particularly left ventricular (LV) hypertrophy. Hypertrophy has been related to the often associated hypertension and little is known about the effect of high cortisol levels on ventricular mass and function. This is the first comprehensive description of biventricular and left atrial volumes and LV mass assessed by CMR in hypercorticism compared to matched controls. Furthermore, the reversibility of the cardiac phenotype associated with hypercorticism was evaluated after treatment.

Cellular Mechanisms of Cardiac Depression and Recovery in Endotoxemic Mice

Sepsis and septic shock are associated with a reversible cardiac dysfunction, that complicates management and worsens prognosis. In patients that survive septic shock, cardiac function recovers spontaneously, through mechanisms that are currently unknown. Here we aimed to identify the intracellular calcium (Ca2+) transporters responsible for cardiac recovery after endotoxemic challenge in mice. Male C57Bl6 mice were administered lipopolysaccharide (LPS, 7 μg/g weight, ip). 12h after LPS administration, cardiomyocyte sarcomere shortening (SS) and Ca2+ transients (ΔCai, measured with fura2-AM) were decreased to 53 ± 10% and 78 ± 5% of control, respectively, in association with a decrease in trans-sarcolemmal Ca2+ influx (Cainf) through the L-type Ca2+ channels (LTCC, to 65± 9%) and sarcoplasmic reticulum (SR) Ca2+ pump (SERCA) reuptake (88 ± 5%, n > 19 cells from 3 mice for all). SR Ca2+ load (CaSR, measured with caffeine) was unchanged, while SR fractional release (FR, as αCai/CaSR) was decreased to 84 ± 6% of control (n's as above). 72h after LPS administration, survival was 40%. In cells isolated from surviving mice 72h after LPS, ΔCa, FR and Cainf were fully recovered, while SERCA showed a supranormal function (138 ± 4% of control, n's as above). SS showed a trend towards a partial depression (to 82 ± 7% of control, p = 0.077, n's as above) at 72h, that persisted up to 6 days after LPS administration. In conclusion, the recovery of cardiac Ca2+ handling after LPS challenge is associated with a full recovery of LTCC dysfunction, a supranormal activation of SERCA, despite, possibly, a persistent dysfunction in the contractile mechanisms downstream of the Ca2+ transient.

Patients with the tako-tsubo cardiomyopathy-clinical evaluation and outcome

ObjectiveTako-tsubo cardiomyopathy (TTC) or is a rare, acute, reversible cardiac dysfunction mimicking an acute coronary syndrome (ACS) and usually connected with a preceding intense physical or emotional stress trigger. This case series-observational study is to evaluate the clinical findings (including the depression and anxiety disorders) and outcome in patients with the tako-tsubo cardiomyopathy treated in our Centre, during 18 month period. MethodsFrom the group of 730 patients, who were admitted with the suspected acute myocardial infarct, ten patients, who fulfilled diagnostic criteria for TTC, were evaluated. For each patient we assessed: clinical characteristic, previous medical history including coronary disease risk factors and preceding stress trigger, 12-leads electrocardiography and laboratory tests. All patients underwent coronary-artery angiography, trans-thoracic echocardiography and completed the questionnaire evaluating the depression and anxiety disorders. ResultsThe estimated prevalence and clinical features of patients with the tako-tsubo cardiomyopathy in our Centre were similar to those in the literature, with the wide range of stress triggers. There was a statistically significant improvement in the ejection fraction during the hospitalization. Psychological tests revealed the 0.7 occurrence of depression or anxiety disorders among our patients. ConclusionsThe exact pathogenesis of the tako-tsubo cardiomyopathy remains uncertain, but it is important to take it into account as a differential diagnosis in patients with the clinical features of myocardial infarct in the absence of coronary artery stenosis.

Factors Affecting Long-Term Safety of Trastuzumab in Patients with Early HER2-Positive Breast Cancer

Background: Trastuzumab treatment is associated with cardiac dysfunction. We evaluated the incidence of cardiotoxicity during and long-term after trastuzumab treatment in an unselected early breast cancer population. Methods: This study included a retrospective part, the chemotherapy- and trastuzumab treatment period and a prospective part, the period of data collection long-term after trastuzumab treatment. Cardiac evaluation included left ventricular ejection fraction (LVEF) changes and an evaluation of symptomatic cardiotoxicity. Cardiac events were defined as a decrease of 10 percentage points in LVEF compared with baseline and to an absolute LVEF of below 50%. Secondary outcomes included the evaluation of cardiac markers (B-type natriuretic peptide and troponins) and single nucleotide polymorphisms (SNPs) in the HER2 gene as parameters to detect or predict trastuzumab-related cardiotoxicity. Results: Overall, 105 patients were evaluable for the primary endpoint. The 3-year cumulative incidence of cardiac events was 12% (95 CI, 4%-19%). All 8 patients with a cardiac event were pre-treated with anthracyclines and cyclophosphamide and 7 of them recovered partially or completely. Four patients experienced symptomatic cardiotoxicity, of who 2 recovered completely and the other 2 recovered partially. No statistically significant association was observed between cardiac events and cardiac markers or SNPs. Conclusion: Trastuzumab treatment in combination with anthracy cline-based chemotherapy is associated with significant and only partly reversible cardiac dysfunction. Baseline LVEF value is a prominent predictor for long-term LVEF especially, in patients who are not treated with anthracycline-based chemotherapy. These findings can be used to establish optimal monitoring strategies in trastuzumab treatment.

Assessment of Adjuvant Trastuzumab-Associated Cardiac Toxicity in Korean Patients with Breast Cancer: A Single-Center Analysis

Background: We performed this analysis to investigate the clinical presentation of trastuzumab-associated cardiac toxicity in Korean women. Method: 124 patients treated in a single institute from January 2006 to November 2011 with adjuvant trastuzumab therapy following primary surgery were identified from a database. We evaluated the cumulative incidence of cardiac toxicity, associated risk factors, and changes in cardiac function during trastuzumab treatment. Results: The median age of patients was 50 years (range 27-73). After 12 months of follow-up, the cumulative incidence of cardiac toxicity was 12.1% (grade I: 8.1%, grade II: 0.8%, grade III: 3.2%). In total, 4% of patients discontinued treatment due to cardiac dysfunction. The left ventricular ejection fraction (LVEF) recovered in all patients who discontinued or delayed treatment due to cardiac dysfunction following treatment discontinuation. The degree of the decrease in LVEF was large at 6 months after the initiation of treatment. A lower LVEF at baseline (<65%) was associated with cardiac toxicity. Conclusions: The low incidence of cardiac toxicity and the reversibility of cardiac dysfunction may validate the safety of trastuzumab treatment in Korean women with an acceptable baseline LVEF.

Reversal of cardiac dysfunction and subcellular alterations by metoprolol in heart failure due to myocardial infarction

In order to examine the reversibility of heart failure due to myocardial infarction (MI) by β-adrenoceptor blockade, 12 weeks infarcted rats were treated with or without metoprolol (50 mg/kg/day) for 8 weeks. The depressed left ventricular (LV) systolic pressure, positive and negative rates of changes in pressure development, ejection fraction, fractional shortening and cardiac output, as well as increased LV end-diastolic pressure in 20 weeks MI animals were partially reversed by metoprolol. MI-induced decreases in septum (systolic) thickness as well as increase in LV posterior wall thickness and LV internal diameter were partially or fully reversible by metoprolol. Treatment of MI animals with metoprolol partially reversed the elevated levels of plasma norepinephrine and dopamine without affecting the elevated levels of epinephrine. Although sarcoplasmic reticular (SR) Ca(2+)-uptake, as well as protein content for SR Ca(2+)-pump and phospholamban, were reduced in the infarcted hearts; these changes were partially reversible with metoprolol. Depressed myofibrillar Ca(2+)-stimulated ATPase activity, as well as mRNA levels for SR Ca(2+)-pump, phospholamban and α-myosin heavy chain, were unaffected whereas increased mRNA level for β-myosin heavy chain was partially reversed by metoprolol. The results suggest that partial improvement of cardiac performance by β-adrenoceptor blockade at advanced stages of heart failure may be due to partial reversal of changes in SR Ca(2+)-pump function whereas partial to complete reverse cardiac remodeling may be due to partial reduction in the elevated levels of plasma catecholamines.

Soluble Epoxide Hydrolase Inhibition Does Not Prevent Cardiac Remodeling and Dysfunction After Aortic Constriction in Rats and Mice

Epoxyeicosatrienoic acids, substrates for soluble epoxide hydrolase (sEH), exhibit vasodilatory and antihypertrophic activities. Inhibitors of sEH might therefore hold promise as heart failure therapeutics. We examined the ability of sEH inhibitors GSK2188931 and GSK2256294 to modulate cardiac hypertrophy, fibrosis, and function after transverse aortic constriction (TAC) in rats and mice. GSK2188931 administration was initiated in rats 1 day before TAC, whereas GSK2256294 treatment was initiated in mice 2 weeks after TAC. Four weeks later, cardiovascular function was assessed, plasma was collected for drug and sEH biomarker concentrations, and left ventricle was isolated for messenger RNA and histological analyses. In rats, although GSK2188931 prevented TAC-mediated increases in certain genes associated with hypertrophy and fibrosis (α-skeletal actin and connective tissue growth factor), the compound failed to attenuate TAC-induced increases in left ventricle mass, posterior wall thickness, end-diastolic volume and pressure, and perivascular fibrosis. Similarly, in mice, GSK2256294 did not reverse cardiac remodeling or systolic dysfunction induced by TAC. Both compounds increased the sEH substrate/product (leukotoxin/leukotoxin diol) ratio, indicating sEH inhibition. In summary, sEH inhibition does not prevent cardiac remodeling or dysfunction after TAC. Thus, targeting sEH seems to be insufficient for reducing pressure overload hypertrophy.

SYMPATHOVAGAL IMBALANCE IN TAKOTSUBO CARDIOMYOPATHY

Takotsubo cardiomyopathy is an acute reversible cardiac dysfunction syndrome associated with high circulating catecholamine levels. Our objective was to investigate whether abnormal cardiovascular control might play a role in the pathophysiology.We studied autonomic cardiovascular reflexes in 10 women who had takotsubo (33±7 months after being hospitalized) and 10 age/BMI matched healthy women.In the women with takotsubo, indices of vagal modulation of heart rate induced by respiration were uniformly reduced (expiratory:inspiratory ratio: p&lt;0.01, pnn50%: p&lt;0.02, rMSSD: p&lt;0.03). Cognitive (stroop test: p&lt;0.03) and emotional arousal (event recall: p&lt;0.05) produced exaggerated pressor responses, without detectable ECG changes. Pressor responses to hemodynamic stimuli were also amplified (Valsalva SBP overshoot: p&lt;0.05). Takotsubo women had increased BP variability in the short‐term (St. Dev. SBP: p&lt;0.01). Ambulatory recordings captured an exaggerated morning surge in SBP after awakening from sleep (p&lt;0.05). Cardiovagal baroreflex gain was significantly lower in the takotsubo women (sequence analysis: p&lt;0.01, regression method: p&lt;0.001, transfer function gain: p&lt;0.001).Women with takotsubo have heightened sympathetic responsiveness, labile BP and reduced vagal modulation of the heart. This shift in sympathovagal balance could play a role in the pathophysiology.

Takotsubo cardiomyopathy: a novel beta-adrenergic blocker withdrawal syndrome

The authors describe two cases of takotsubo cardiomyopathy developing after an abrupt withdrawal of carvedilol and bisoprolol. Takotsubo or stress cardiomyopathy is characterized by acute and reversible cardiac dysfunction without coronary artery disease. It is triggered by acute emotional or physical stress, drugs or drug withdrawal. The immediate discontinuation of the long acting vasodilator beta-blocker, carvedilol has not yet been described to cause takotsubo cardiomyopathy. The authors recommend cautious withdrawal of beta-blockers.

Reversible cardiac dysfunction associated with hypocalcemia: a systematic review and meta-analysis of individual patient data

Case reports have documented reversible cardiac dysfunction in the setting of severely depressed extracellular calcium concentrations. The present systematic review and meta-analyses of individual patient data were conducted to further characterize the cardiac dysfunction associated with low serum calcium levels in the clinical setting. We searched Ovid MEDLINE, Embase, PubMed databases and the Cochrane Library and the Registry of Clinical Trials from 1948 through August 2011. Studies that evaluated low serum calcium and cardiac dysfunction were identified and included for review. A total of 43 studies comprised of 47 individual cases met inclusion criteria. Univariate linear regression analysis showed a statistically significant correlation between corrected QT interval (QTc) length and corrected total serum calcium level (B = -23.19, SE = 8.04, P = 0.01), left ventricular ejection fraction and corrected total serum calcium (B = 5.16, SE = 1.29, P < 0.01) and ionized serum calcium (B = 5.48, SE = 2.04, P = 0.03). Hypocalcemia may be associated with reversible cardiac dysfunction including QTc interval prolongation and depressed left ventricular systolic function. The available evidence is very limited and does not provide a rationale for a certain threshold or a recommendation for calcium replacement. Future research is needed in this important and common metabolic disorder.

Rationale and design of a randomized trial on the impact of aldosterone antagonism on cardiac structure and function in diabetic cardiomyopathy

Development of a cardiomyopathy in diabetes mellitus is independent of traditional risk factors, with no clinical trials targeting specific therapeutic interventions. Myocardial fibrosis is one of the key mechanisms and aldosterone is a key mediator of myocardial fibrosis. We propose that aldosterone antagonism will improve cardiac function. We aim to evaluate the efficacy of selective aldosterone receptor antagonism with eplerenone added to optimal medical treatment in improving cardiac structure and function in diabetic cardiomyopathy. We will randomize 130 patients with type 2 diabetes mellitus, stable metabolic control and impaired left ventricular (LV) systolic or diastolic function, to either eplerenone (target dose 50mg) or matching placebo, in addition to optimal medical therapy for 12 months. The primary endpoints are changes in LV systolic and diastolic function, measured by echocardiographic 2-dimensional speckle tracking strain and strain rate and tissue Doppler imaging. The secondary endpoints include changes in echocardiographic markers and plasma biomarkers of collagen turnover; left atrial dimensions and function, incidence of atrial fibrillation and changes in exercise capacity and dyspnea score. The present study will assess whether specific aldosterone antagonism with eplerenone in addition to standard therapy will prevent progression or reverse cardiac dysfunction in diabetic cardiomyopathy using sensitive, robust and quantifiable echocardiographic measures that allow early detection of change. The study may offer a new direction in the management of this condition.Trial registrationACTRN12610001063000

Cardiomyopathies in Tropical Countries: Causes and Nosological Perspective

Background: Cardiomyopathy is the main cause of heart failure in developing countries, mainly in Africa. In those areas the concept of “tropical cardiomyopathy” is still used to design all unexplained cardiomyopathy. The primary aim of this review is first to review the main etiologies of cardiomyopathies observed in tropical countries and second to gain a better understanding of the nosological place of the so-called “tropical cardiomyopathies” in the current framework of cardiomyopathies. Methods and Results: We reviewed relevant references over the last forty years (June, 1976 to May 2012). Given literature data, endomyocardial fibrosis (EMF) is mainly diagnosed in sub-Saharan countries, as well as Brazil and India. Peripartum cardiomyopathy (PPCM) is observed with a higher prevalence than in temperate countries. Sickle cell anemia does not induce specific cardiomyopathy in all echocardiographic studies. Malnutrition and chronic anemia can induce reversible cardiac dysfunction. Myocardial involvement in parasitic infections is restricted to Chagas disease and probably to human African trypanosomiasis. Helminthiasis is not involved in the pathogenesis of cardiomyopathy except for the deleterious effect of high eosinophilia induced by some endemic diseases (filariasis, schistosomiasis). Primary cardiomyopathies (dilated, hypertrophic, and restrictive cardiomyopathy) have no specificity. Arrhythmogenic right ventricular dysplasia and left ventricular noncompaction are also reported and do not differ from elsewhere. Conclusions: The concept of tropical cardiomyopathy is no longer relevant as most of the cardiomyopathies observed in tropical countries have no specificity, with few exceptions (PPCM, EMF, Chagas disease). In this context, the European Society of Cardiology classification offers a simpler clinical approach and allows the inclusion of the rare tropical specificities.

Stress-Induced Cardiomyopathy (Takotsubo Cardiomyopathy) After Liver Transplantation—Report of Two Cases

Cardiac complications after liver transplantation are a common cause of death. Stress-induced cardiomyopathy, also called takotsubo cardiomyopathy, is a special form of cardiomyopathy that is precipitated by a stress situation. It can occur after a surgical procedure that results in acute heart failure. Herein we have presented 2 cases of reversible stress-induced cardiac dysfunction early in the period after liver transplantation. Before surgery, cardiac evaluation was normal, with both patients classified as low risk for cardiovascular events during the proposed procedure. Both patients experienced cardiac arrest after graft reperfusion with return of spontaneous circulation after resuscitation. Their early periods after transplantation were characterized by cardiogenic shock secondary to important ventricular dysfunction requiring vasoactive drugs. Subsequent investigations excluded coronary disease. The diagnosis of takotsubo cardiomyopathy was established based on the clinical features and ancillary tests, particularly echocardiography showing apical ballooning. In both cases, ventricular function recovered completely. In conclusion, stress-induced cardiomyopathy, an underestimated cause of heart complications, should be considered as a possible cause of cardiac failure in liver transplant patients.

Abstract 164: MicroRNA-29c Reduces Serca2 Expression During Myocardial Hypoxia

The cardiac response to a hypoxic challenge is coordinated by the transcription factor Hypoxia Inducible Factor-1 (HIF-1), which drives the transcription of a large number of genes pertinent to angiogenesis, metabolism, and calcium cycling. Expression of HIF-1alpha that has been mutated to remove oxygen regulation recapitulates many of the changes in gene expression seen in hypoxia. It also results in reversible cardiac dysfunction associated with marked decrease of Sarco-Endoplasmic Reticulum Calcium-Dependent ATP-ase (SERCA2). This decrease in SERCA was more rapid and more substantial than a moderate decrease seen in the mRNA for this protein. In this study, we tested the hypothesis that the decrease in SERCA2 is mediated by the up-regulation of microRNA (miRNA) in the heart. We identified 30 miRNAs that are dysregulated upon induction of oxygen stable HIF1 expression. Three of these have evident binding sites in the 3’ untranslated region of the SERCA2 gene. Transient co-transfection of a mimic molecule for these three miRs with a luciferase reporter construct that includes the 3’ UTR of SERCA2 showed that mi-29c produced a substantial decrease in reporter expression. This effect is abolished by the mutagenesis of the predicted target site within the 3’UTR. Similarly, transfection of this mimic molecule into a cell line that expresses SERCA2 results in a reduction in SERCA2 protein levels. An antagomir to this miR rescues the reduction in SERCA seen with HIF expression. We conclude that miR-29c, is responsible for an important portion of the down-regulation of SERCA2, and thus the contractile dysfunction, seen in hypoxia.

Myo-Pericarditis and Congestive Heart Failure Secondary to Mesalamine Use Associated With Completely Reversible Cardiac Dysfunction

Mesalamine is a 5-ASA d erivative commonly used to treat ulcerative colitis and mild to moderate crohn’s disease. Rarely, it has been associated with myocarditis or pericarditis. Several hypotheses have been proposed but the exact mechanism of cardiac injury is still unclear. We present a case of combined pericarditis and myocarditis in a young man on mesalamine therapy, with subsequent deterioration of cardiac function, EKG changes and signs of congestive heart failure. After the appropriate treatment, beginning with discontinuation of mesalamine, he had complete recovery of cardiac function to normal. This case exemplifies the importance of quick physician recognition of the disease association and immediate discontinuation of the drug for more successful outcomes in conjunction with appropriate management. doi:10.4021/jmc617w

Preservation of Myocardium During Coronary Artery Bypass Surgery

Myocardial protection aims to prevent reversible post-ischemic cardiac dysfunction (myocardial stunning) and irreversible myocardial cell death (myocardial infarction) that occur as a consequence of myocardial ischemia and/or ischemic-reperfusion injury. Although the mortality rate for isolated coronary artery bypass grafting has been markedly reduced during the past decade, myocardial death, as evidenced by elevation in creatine kinase-myocardial band and/or cardiac troponin, is common. This is ascribed to suboptimal myocardial protection during cardiopulmonary bypass or with off-pump technique, early graft failure, distal embolization, and regional or global myocardial ischemia during surgery. An unmet need in contemporary coronary bypass surgery is to find more effective cardioprotective strategies that have the potential for decreasing the morbidity and mortality associated with suboptimal cardioprotection. In the present review article on myocardial protection in contemporary coronary artery bypass surgery, we attempt to elucidate the clinical problems, summarize the outcomes of selected phase III trials, and introduce new perspectives.

Can we make sense of takotsubo cardiomyopathy? An update on pathogenesis, diagnosis and natural history

Takotsubo cardiomyopathy (TTC) is a form of reversible acute cardiac dysfunction of uncertain pathogenesis, which occurs predominantly in postmenopausal women, often with antecedent severe stress. Systolic dysfunction most commonly affects the apex of the left ventricle. There is considerable uncertainty regarding the pathogenesis of TTC and the optimal diagnostic methodology. Acute catecholamine release may play a component role, but the regional hypokinesis is associated with an acute inflammatory process, with resultant early release of brain natriuretic peptide (BNP) and N-terminal pro-BNP. As the diagnosis of TTC has largely been a process of exclusion, there has been considerable underdiagnosis. The combination of demographics, preceding history, ECG appearances and N-terminal pro-BNP elevation may provide the basis for improved early diagnosis. Complete recovery takes at least several months, with a risk of recurrent episodes. Efforts to delineate pathogenesis, expedite diagnosis and evaluate residual disability may assist in the development of appropriate treatment regimens.

Acute non-ST elevation myocardial infarction following paclitaxel administration for ovarian carcinoma: A case report and review of literature

We report a case of an acute non-ST elevation myocardial infarction (AMI) induced by paclitaxel in a patient with ovarian cancer. A 45-year-old premenopausal lady without any co-morbidity was started on the first cycle of neoadjuvant chemotherapy with paclitaxel-based regimen for advanced stage ovarian cancer. The patient developed chest pain 3 h after paclitaxel infusion with characteristic electrocardiographic changes of antero-apical myocardial infarction. The patient recovered on conservative medical management with reversion of electrocardiogram (ECG) changes. Cardiac ischemia and myocardial infarction, possibly due to coronary vasospasm, are rare adverse effects of paclitaxel with reported incidence of 0.26%. We have reported a case of paclitaxel-induced myocardial infarction with reversible cardiac dysfunction. The possibility of myocardial infarction should be considered in patients who develop chest pain or other symptoms after paclitaxel infusion.