Fracture and plastering of distal left main stent during double-kissing Culotte technique: a case report.

Background: Acute fracture of a left main (LM) stent during angioplasty is a rare complication. Cardiologists should be aware of the risk of stent fracture (SF) following kissing balloon inflation (KBI) even if the effective diameter of the balloons does not exceed the recommended expansion limits of stents. Case summary: A 64-year-old female with hypertension and dyslipidaemia presented with crescendo angina since three months in spite of optimal medical therapy. Coronary angiogram showed a distal LM bifurcation lesion. The patient was admitted for LM bifurcation stenting by upfront two-stent technique (inverted double-kissing Culotte technique). Following first KBI of the stent placed from left circumflex artery (LCX) to LM, there was stent deformation in the LM shaft. As we had planned the Culotte technique, we decided to exclude the fractured segment by stenting from left anterior descending artery (LAD) to LM. The stent from LAD-LM successfully excluded the fractured part of the first stent from the lumen of LM. Optical coherence tomography done after final KBI from LCX-LM revealed successful exclusion of the deformed segment of the LCX stent with mild malapposition at the site of the deformed stent. A follow-up angiogram after six months showed normal in-stent flow with no evidence of restenosis or pseudoaneurysm. Discussion: Acute LM SF during coronary intervention can occur even if the effective cumulative diameter of the inflated balloons does not exceed the mentioned expansion limit of stents. Intravascular imaging is a helpful modality to define type of SF and its management.

Balloon mitral valvuloplasty in low gradient severe rheumatic mitral stenosis: Immediate and short-term outcomes.

Background: Efficacy of balloon mitral valvuloplasty (BMV) in low gradient severe rheumatic mitral stenosis (MS) is not very well defined. This study was undertaken to evaluate the outcomes of BMV in low gradient severe rheumatic MS. Methods: Severe MS was defined as mitral valve area < 1.5 cm2. Low gradient was defined as mean diastolic trans-mitral gradient (MG) < 10 mmHg and low flow as stroke volume index < 35 ml/m2 on echocardiography. Sixty patients were divided into normal-flow/low-gradient (NFLG) (40) and low-flow/low-gradient (LFLG) (20) groups. Post-BMV parameters were recorded after 72 h and at the end of one year. Results: Mean age was 36.2 ± 6.6 years in NFLG group and 40.6 ± 2.6 years in LFLG group (p < 0.01) and females were 75 % (n = 30) in NFLG group as compared to 60 % (n = 12) in LFLG group. Patients in the LFLG group had higher Wilkins score (p < 0.02) and prevalence of atrial fibrillation (n = 8, 40 %) as compared to NFLG group (n = 7, 17.5 %; p < 0.01). A greater decrease in MG was observed in NFLG group (p < 0.01), whereas increase in MVA was comparable in both the groups (p > 0.05). Ninety percent (n = 36) patients improved in NFLG group in comparison to 70 % (n = 14) in LFLG group (p < 0.01). At the end of one-year, symptomatic improvement persisted in all patients who became asymptomatic post-BMV. Conclusion: Symptomatic improvement following BMV was better seen in NFLG group because of greater decrease in MG in comparison to LFLG group. Results of BMV were suboptimal in LFLG group because of higher sub-valvular obstruction, increased age and higher prevalence of AF.

Novel lipid biomarkers and associated gene polymorphism in young ST-segment elevation myocardial infarction.

BACKGROUND: There is an increasing prevalence of coronary artery disease (CAD) in younger individuals. Lipid biomarkers such as lipoprotein-a (Lp-a), Apo A1, Apo B and Paraoxonase-1 (PON1) serve as important risk predictors for development of CAD. There is little evidence regarding the role of lipid biomarkers and their genetic polymorphisms in young (<50 years) ST-segment elevation myocardial infarction (STEMI) patients. METHODS: This study included 110 young (18-50 years) STEMI patients and 110 healthy controls. Serum levels of Apo A1, Apo B, Paraoxonase-1 (PON-1) and Lipoprotein-associated phospholipase A2 (Lp-PLA2) were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) genes were evaluated. RESULTS: Serum levels of apo B (101.31 ± 27.58 vs 75.31 ± 18.77 mg/dl; p < 0.0001), Lp(a) [87.56 ± 74.28 vs 25.81 ± 24.66 mg/dl, p < 0.0001] and Lp-PLA2 [5.97 ± 1.39 vs 3.49 ± 1.27 ng/mL, p < 0.0001] were significantly higher in patients as compared to controls. Serum levels of Apo A1 [44.76 ± 35.65 vs 95.97 ± 29.89; p < 0.0001] and PON1 [2.63 ± 1.5 vs 3.87 ± 1.47 ng/mL, p < 0.0001] were significantly lower in cases as compared with controls. Additionally, patients with genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) gene had an increased risk of STEMI. CONCLUSION: Lipid biomarkers such as Apo A1, Apo B and PON1 and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals.

Matrix metalloproteinases and their gene polymorphism in young ST-segment elevation myocardial infarction.

BACKGROUND: Genetic polymorphism in MMPs are associated with multiple adverse CV events. There is little evidence regarding role of MMPs and their genetic polymorphisms in young (<50 years) ST-segment elevation myocardial infarction (STEMI) patients. METHODS: This study included 100 young (18-50 years) STEMI patients and 100 healthy controls. Serum levels of MMP-3, MMP-9 and TIMP were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the MMP-9 gene (-1562 C/T and R279Q) & MMP-3 gene (5A/6A-1612) was evaluated. All these patients were followed up for one year and major adverse cardiac events (MACE) were determined. RESULTS: Serum levels of MMP-3 (128.16 ± 115.81 vs 102.3 ± 57.28 ng/mL; P = 0.04), MMP-9 (469.63 ± 238.4 vs 188.88 ± 94.08 pg/mL; P < 0.0001) and TIMP (5.84 ± 1.93 vs 2.28 ± 1.42 ng/mL; P < 0.0001) were significantly higher in patients as compared to controls. Additionally, patients with genetic polymorphisms in the MMP genes (5A/5A, 6A/6A and the AG genotypes) had an increased risk of STEMI. Patients with MACE had significantly higher levels of MMP-9 (581.73 ± 260.93 vs 438.01 ± 223.38 pg/mL; P = 0.012). A cutoff value of 375.5 pg/mL of MMP-9 was best able to discriminate patients with STEMI and MACE with sensitivity of 77.3% and specificity of 57%. CONCLUSION: Novel biomarkers such as MMP-3, MMP-9 and TIMP and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals. Higher MMP-9 levels in STEMI patients with MACE suggests its potential role in predicting cardiac remodeling and left ventricular dysfunction.

COVID-19 induced ventricular tachycardia storm unmasking a clinically silent cardiomyopathy: a case report.

BACKGROUND: Coronavirus disease (COVID-19) is a systemic illness characterized by raging impact of cytokine storm on multiple organs. This may trigger malignant ventricular arrhythmias and unmask a clinically silent cardiomyopathy. CASE SUMMARY: A 57-year-old gentleman, known case of hyperthyroidism and diabetes, was referred to our emergency department with history of two ventricular tachycardia (VT) episodes requiring direct current cardioversion in last 3 h followed by another episode in our emergency department that was cardioverted. There was no past history of cardiac illness. His 12-lead electrocardiogram (during sinus rhythm) along with screening echocardiography suggested Arrhythmogenic right ventricular cardiomyopathy (ARVC). He was coincidentally found to be COVID-19 positive by reverse transcription-polymerase chain reaction (RT-PCR) as part of our routine screening. However, he had no fever or respiratory complaints. We noted raised systemic inflammatory markers and cardiac troponin T which progressively increased over the next 4 weeks paralleled by an increase in ventricular premature contraction burden and thereafter started decreasing and returned to baseline by 6th week when the patient became COVID-19 negative by RT-PCR. Subsequently, a single-chamber automated implantable cardioverter-defibrillator implantation was done following which there was a transient increase in these biomarkers that subsided spontaneously. The patient is asymptomatic during 6 weeks of follow-up. DISCUSSION: COVID-19-associated cytokine surge triggering VT storm and unmasking a clinically silent ARVC has not yet been reported. The case highlights a life-threatening presentation of COVID-19 and indicates a probable link between inflammation and arrhythmogenicity.

Novel lipid biomarkers and associated gene polymorphism in young ST-segment elevation myocardial infarction

Background: There is an increasing prevalence of coronary artery disease (CAD) in younger individuals. Lipid biomarkers such as lipoprotein-a (Lp-a), Apo A1, Apo B and Paraoxonase-1 (PON1) serve as important risk predictors for development of CAD. There is little evidence regarding the role of lipid biomarkers and their genetic polymorphisms in young (<50 years) ST-segment elevation myocardial infarction (STEMI) patients. Methods: This study included 110 young (18e50 years) STEMI patients and 110 healthy controls. Serum levels of Apo A1, Apo B, Paraoxonase-1 (PON-1) and Lipoprotein-associated phospholipase A2 (Lp-PLA2) were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) genes were evaluated. Results: Serum levels of apo B (101.31 ± 27.58 vs 75.31 ± 18.77 mg/dl; p < 0.0001), Lp(a) [87.56 ± 74.28 vs 25.81 ± 24.66 mg/dl, p < 0.0001] and Lp-PLA2 [5.97 ± 1.39 vs 3.49 ± 1.27 ng/mL, p < 0.0001] were significantly higher in patients as compared to controls. Serum levels of Apo A1 [44.76 ± 35.65 vs 95.97 ± 29.89; p < 0.0001] and PON1 [2.63 ± 1.5 vs 3.87 ± 1.47 ng/mL, p < 0.0001] were significantly lower in cases as compared with controls. Additionally, patients with genetic polymorphisms in the Apo A1 (75G/A) and the PON1 (Q192R) gene had an increased risk of STEMI. Conclusion: Lipid biomarkers such as Apo A1, Apo B and PON1 and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals.

Matrix metalloproteinases and their gene polymorphism in young ST-segment elevation myocardial infarction

Background: Genetic polymorphism in MMPs are associated with multiple adverse CV events. There is little evidence regarding role of MMPs and their genetic polymorphisms in young (<50 years) STsegment elevation myocardial infarction (STEMI) patients. Methods: This study included 100 young (18e50 years) STEMI patients and 100 healthy controls. Serum levels of MMP-3, MMP-9 and TIMP were estimated for both patients as well as controls. Additionally, genetic polymorphisms in the MMP-9 gene (_x0001_1562 C/T and R279Q) & MMP-3 gene (5A/6A-1612) was evaluated. All these patients were followed up for one year and major adverse cardiac events (MACE) were determined. Results: Serum levels of MMP-3 (128.16 ± 115.81 vs 102.3 ± 57.28 ng/mL; P ¼ 0.04), MMP-9 (469.63 ± 238.4 vs 188.88 ± 94.08 pg/mL; P < 0.0001) and TIMP (5.84 ± 1.93 vs 2.28 ± 1.42 ng/mL; P < 0.0001) were significantly higher in patients as compared to controls. Additionally, patients with genetic polymorphisms in the MMP genes (5A/5A, 6A/6A and the AG genotypes) had an increased risk of STEMI. Patients with MACE had significantly higher levels of MMP-9 (581.73 ± 260.93 vs 438.01 ± 223.38 pg/mL; P ¼ 0.012). A cutoff value of 375.5 pg/mL of MMP-9 was best able to discriminate patients with STEMI and MACE with sensitivity of 77.3% and specificity of 57%. Conclusion: Novel biomarkers such as MMP-3, MMP-9 and TIMP and their genetic polymorphism are associated with the susceptibility for STEMI in young individuals. Higher MMP-9 levels in STEMI patients with MACE suggests its potential role in predicting cardiac remodeling and left ventricular dysfunction