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Introduction: Aluminum phosphide (ALP) is a pesticide that is highly toxic. It is a mitochondrial toxin that causes death by cardiac and metabolic toxicity. The most ominous effect is cardiac toxicity, which may range from minor electrocardiographic abnormalities to severe depression of cardiac contractility secondary to toxic myocarditis. There is no documented report of the use of Intra-aortic Balloon Pump (IABP) for toxic myocarditis from ALP poisoning, although it has been used effectively for toxic myocarditis due to other toxins.Case Report: We are reporting a young female who presented with ALP poisoning, in cardiogenic shock due to myocarditis. We used an IABP for cardio-circulatory support until the effects of ALP resolved. She is the only reported survivor of ALP poisoning, presenting with cardiogenic shock.Discussion: Several reports describe the use of IABP for cardiogenic shock due to toxic myocarditis. There is no report in the medical literature using IABP for cardiogenic shock caused by ALP toxin-induced myocarditis. Our patient presented with cardiocirculatory shock, necessitating the use of inotropes and mechanical ventilation. As she did not improve despite ventilation and maximal doses of inotropes, IABP was used for cardio-circulatory support until the effects of ALP resolved.

The normal left ventricular shape has been defined as prolate ellipsoid. This shape is an adaptation to evolution. A knowledge of its unique macro and micro architecture forms the cornerstone in the understanding of its complex function. The left ventricle has a unique architecture with three different myofiber orientations, the longitudinal, circumferential and oblique fibers. The oblique orientation of fibers is essential for effective clockwise and anticlockwise torsional movements during systole and diastole, for optimal ventricular ejection and filling. The orientation and fiber angle decide the shape of the ventricle. An ellipsoid shape is vital for optimal function. Pathological disease states such as ischemic heart disease, valvular heart disease and cardiomyopathies cause a loss of obliquity of the myofibers. The myofibers become more horizontal resulting in ventricular dilatation and increased sphericity. The change from ellipsoid to globular shape with disease heralds the onset of left ventricular dysfunction and initiates the cascade of heart failure. Several strategies have been successful in reverting ventricular dilatation and sphericity to a more ellipsoid geometry. Pharmacological therapies like beta blockade and angiotensin converting enzyme inhibition have proven beneficial in early stages of heart failure with pathological remodeling. However, these agents in isolation are limited in reversing pathological remodeling in advanced heart failure. In some cases of advanced heart failure due to postinfarction left ventricular aneurysms, ventricular volume reduction with restoration surgeries have a role in restoring ventricular geometry with beneficial clinical outcomes. Surgical ventricular restoration has progressively evolved from the 1950s. Initially, aneurysmal resection and linear repair was done. This was gradually replaced by endoventricular patch plasty, which had better results. The resulting left ventricle was smaller in size but still continued to have a spherical configuration. Exclusion of the infarct area with a smaller longitudinal patch results in realignment of the non-diseased ventricular fibers with a resulting ellipsoid shape. This ellipsoid shape ensures clinical benefits. The geometry of the endoventricular patch thus holds the key to optimal ventricular shape in these patients. The technique to optimally restore a diseased ventricle to normal continues to evolve. This requires insights into the normal architecture and function, and the pathophysiologic effects of disease.

BACKGROUND Guidelines recommend nonstatin lipid-lowering agents in patients at very high risk for major adverse cardiovascular events (MACE) if low-density lipoprotein cholesterol (LDL-C) remains ≥70 mg/dL on maximum tolerated statin treatment. It is uncertain if this approach benefits patients with LDL-C near 70 mg/dL. Lipoprotein(a) levels may influence residual risk. OBJECTIVES In a post hoc analysis of the ODYSSEY Outcomes (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab) trial, the authors evaluated the benefit of adding the proprotein subtilisin/kexin type 9 inhibitor alirocumab to optimized statin treatment in patients with LDL-C levels near 70 mg/dL. Effects were evaluated according to concurrent lipoprotein(a) levels. METHODS ODYSSEY Outcomes compared alirocumab with placebo in 18,924 patients with recent acute coronary syndromes receiving optimized statin treatment. In 4,351 patients (23.0%), screening or randomization LDL-C was <70 mg/dL (median 69.4 mg/dL; interquartile range: 64.3–74.0 mg/dL); in 14,573 patients (77.0%), both determinations were ≥70 mg/dL (median 94.0 mg/dL; interquartile range: 83.2–111.0 mg/dL). RESULTS In the lower LDL-C subgroup, MACE rates were 4.2 and 3.1 per 100 patient-years among placebo-treated patients with baseline lipoprotein(a) greater than or less than or equal to the median (13.7 mg/dL). Corresponding adjusted treatment hazard ratios were 0.68 (95% confidence interval [Cl]: 0.52–0.90) and 1.11 (95% Cl: 0.83–1.49), with treatment-lipoprotein(a) interaction on MACE ( P interaction = 0.017). In the higher LDL-C subgroup, MACE rates were 4.7 and 3.8 per 100 patient-years among placebo-treated patients with lipoprotein(a) >13.7 mg/dL or ≤13.7 mg/dL; corresponding adjusted treatment hazard ratios were 0.82 (95% Cl: 0.72–0.92) and 0.89 (95% Cl: 0.75–1.06), with P interaction = 0.43. CONCLUSIONS In patients with recent acute coronary syndromes and LDL-C near 70 mg/dL on optimized statin therapy, proprotein subtilisin/kexin type 9 inhibition provides incremental clinical benefit only when lipoprotein(a) concentration is at least mildly elevated. (ODYSSEY Outcomes: Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab; NCT01663402 )

The relationship of right ventricular function and pulmonary systolic pressure in patients with congestive heart failure was evaluated to risk-stratify them. The study included 147 consecutive patients with symptomatic heart failure who underwent clinical and laboratory examination and echocardiography including Doppler tissue echocardiography. They were followed for a mean of 11.2AE6.4 months. During follow-up, 16 patients died and 45 patients had nonfatal cardiac events. There were 60 readmissions for heart failure. Pulmonary artery systolic pressure and right ventricular systolic function were inversely related (r 2 =0.66, P<.001). On Cox multivariate survival analysis, early worsening of pulmonary arterial pressures was an independent prognostic predictor (hazard ratio, 0.44; confidence interval, 0.28-0.91, P=.024). The patients with pulmonary hypertension and right ventricular systolic dysfunction had the worst prognosis. The assessments of right ventricular function help to risk-stratify patients with heart failure. The early worsening of pulmonary hypertension is a powerful predictor of worse prognosis. Prev Cardiol. 2010;13:72-77.

Surgical ventricular restoration improves cardiac function in patients with large left ventricular aneurysms. Aneurysm repair techniques have evolved to geometric repair by exclusion of the aneurysmal area with a circular patch. But even circular endoventricular patchplasty may result in a less elliptical ventricle. We modified the techniques of both linear and geometric repair. The early and intermediate outcomes in 102 patients with post-infarction left ventricular aneurysm, treated between 2001 and 2004, were analyzed. Concomitant procedures included coronary artery bypass grafting in 73 patients, mitral valve repair in 29, cryoablation in 3, and post-infarction ventricular septal rupture repair in 3. Overall mortality was 12.7%. Left ventricular ejection fraction increased significantly postoperatively, from 31.5% +/- 6.5% to 34.2% +/- 5.9%. There were significant decreases in end-diastolic volumes from 140.3 +/- 38.3 to 100.8 +/- 33.5 mL, and end-systolic volumes from 95.1 +/- 26.1 to 66.0 +/- 21.7 mL. These benefits continued at the 12- to 52-month follow-up. Our modified technique restores a near physiological left ventricular geometry and has a favorable clinical outcome.

Linear endoventricular patch plasty restored a physiological elliptical ventricular geometry with persistent late reverse remodeling. The decreases in EDVs following surgery were significantly linearly proportional to the decreases in SVs at rest, which conforms to the normal left-ventricular geometry.

SVR by geometric repair using a rectangular intracavitary patch helps restoration of a physiological apex with normalization of apical rotation reflecting a near-physiological LV function.